I will be talking about ultrasound evaluation of the aorta and the mesenteric arteries. So starting with abdominal aortic aneurysms, in the United States it's estimated that up to 7% of all adults over the age of 60 have a AAA, and this amounts to about 2.7 million people in our country. These are much more common in men than in women. The incidence increases with age. Other risk factors include having a family history, which is defined as a first-degree relative. Smoking increases your risk of just about everything, and other risk factors include connective tissue disease, hypertension, elevated cholesterol, atherosclerosis, trauma, as well as infection. Very important to know how to measure an abdominal aortic aneurysm and to understand the definition. By convention, somebody is considered to have a AAA if their aorta measures greater than three centimeters of maximal dimension or is more than one and a half times the diameter of the proximal segment. You always measure the aorta from outer wall to outer wall. Most of us focus on a longitudinal image, either coronal or sagittal plane, and you should make your measurement, as you see in these examples here and here along the yellow line in a plane that is perpendicular to the long axis of the lumen. But I want to remind you that aneurysms are three-dimensional features, and so you really do need the transverse plane if we're going to assess any lateral bulging, as you see here. And so we generally recommend that you measure these in two orthogonal planes. Aneurysms are a systemic problem, and if you have an aneurysm one place, you may well have an aneurysm someplace else. And since many patients today are going to be treated with an endograft repair, the landing sites are in the common iliac artery, so you always want to evaluate the common iliac arteries to see if there's an aneurysm there, because if there is, this needs to be excluded as well as the bigger aneurysm in the abdomen. And in this case, you can see this patient with a huge abdominal aortic aneurysm does indeed have a four-centimeter aneurysm involving the right common iliac artery. And the clinicians need to know about that, because they want to make sure the endograft goes through that and ends up in the normal diameter artery distal to this aneurysm, so that aneurysm is excluded and treated as well. You also want to describe your aneurysms in relationship to the renal arteries, because this affects management also. And it is much easier to treat with endograft repair an aneurysm that is below the level of the renal arteries or infrarenal. So here, you can see the aneurysm is nowhere in sight on this transverse image. The order is normal at the origin of both the right and left renal artery. The problem with this plan is that sometimes it's really hard to find the origins of both renal arteries. So a little tip I want to leave you with is that if the aneurysm begins more than two centimeters below the SMA, which you ought to be able to see in everybody, it is usually infrarenal. Now, you can treat juxtarenal and suprarenal aneurysms with endografts, but it is more complicated. They have to do chimney extensions. So it is important to recognize what those look like. And here are two cases where you can see the slide on the left, the big aneurysm here. That encompasses the origin of the right renal artery, a little thrombus in it as well. And here is an even bigger aneurysm with some peripheral thrombus at the level of the left renal artery. So these will be called juxtarenal aneurysms. Now these two aneurysms extend well above the level of the intrarenal arteries, reaching actually up to the diaphragm. So these are suprarenal AAAs. And these are important because these patients, you don't know where the top of the aneurysm is. It's probably in the chest someplace, and so they should have a chest CT for a complete evaluation. Now as you all know, the risk of rupture is related not only to size, but to the rate of growth. And in men, the risk is considered significant once the aneurysm is more than five or five and a half centimeters in diameter, or if there is growth of more than half a centimeter in six months or a centimeter in a 12-month period. Now aneurysms behave a little bit differently in women. First of all, they tend to occur in older women. And even though they are much less common than in men, the risk of rupture is significantly higher, four times as high, and rupture tends to occur at a smaller diameter. Even worse, women have a poorer survival rate, worse by a factor of two, for both emergent as well as elective repair. And so because of this, most people recommend that in a woman you would intervene at a smaller diameter, probably at about four and a half centimeters. The mortality rate following rupture is extremely high, at least 60%. But following elective repair, it is much lower, probably less than 5% for open repair and no more than 2% for endovascular repair. So the only rational conclusion you make is that if you had a screening program and you identify aneurysms and you fix them on an elective basis rather than waiting for them to rupture, you could prevent death from rupture of AAA. And so because of this, screening for abdominal aortic aneurysms actually became a recognized part of the Welcome to Medicare physical and is now available as a one-time screen for patients over the age of 65, provided if you are male that you have a family history or a smoking history, and if you are female that you have a family history. And if you are going to use the billing code for a screening aneurysm as part of the Welcome to Medicare physical, you need to document that history in the report in order to get reimbursed. There is very good epidemiologic data that these screening programs actually do work and have a significant impact on patient outcome. This is a study that was reported out of the United Kingdom. Now it took only men. Remember, the incidence is six times higher in men than in women. Over the age of 65, they defined an aneurysm as being greater than three centimeters and they intervened with surgery. This was published in 2002 before endograft repair was widely available. But they intervened once the aneurysm was greater than 5.5 centimeters in diameter. And in this study, this intervention decreased the risk of AAA-related mortality by 42 percent. About three years later, a similar study was reported out of Scandinavia, and in this study the AAA-related mortality was decreased by 67 percent by their screening program. So this is very, very powerful data that screening for AAAs really does affect outcome. Now if somebody has an aneurysm, you have two approaches to treat it, the open repair or the endovascular repair. And when you compare those two, you notice on lots and lots of data have shown that the short-term mortality and morbidity as well as the long-term outcomes are either better or equivalent for endovascular repair when you compare it to open repair. And so the bottom line is that now endovascular repair is the preferred method of treatment for AAAs provided that the anatomy is appropriate. Now the only caveat about that is that in order to achieve those outcomes, more intervention is required in the endovascular aortic repair group. And this is due to the problem of dealing with endolinks. And endolinks occur primarily because of one of three factors, either structural failure, graft migration, or continued growth of the aneurysm despite the presence, the placement of the endoluminal graft. And occasionally these grafts thrombose. So the bottom line is that if somebody commits to having endovascular repair, they need to commit to lifelong surveillance. So these people really can't be friends of Elon Musk or Jeff Bezos and be planning to go to Mars for 13 years. Now how do you follow these patients? Well, the gold standard for years has been CT surveillance. But the problem with this is that it's expensive. There's a significant risk of nephrotoxicity, and there is also significant radiation exposure. And interestingly enough, there is now a large body of evidence that's accumulated that color Doppler ultrasound surveillance is probably adequate for follow-up of patients at least at low risk for endolinks. Now nobody thinks that color Doppler ultrasound is going to detect all links, all endolinks. But it will detect all that are clinically significant. You are either going to directly see the endolink on color Doppler, or you're going to see that the sac increases in size. And at that point, you can proceed to a CTA. So because of this data, the Society of Vascular Surgery revised their guidelines in 2018. And they recommend the following. You should get an initial baseline CTA at one month. And if it is abnormal, you need to continue to follow the patient with CTA. But if there is no endolink, no increase in size or risk factors, then you can do either a CTA or ultrasound, which means, of course, you would choose to do the ultrasound because it's cheaper and has much less risk to it. And then only if the ultrasound is abnormal would you move to a CTA. And they said, well, we don't really know. We'll see what's going on. So maybe we ought to get a CTA every five years or so just to be on the safe side. So here are a couple of examples. This patient had their graft placed in 2007, was lost to follow-up, returned in 2010. And you can see that that aneurysm increased in size from 6.6 centimeters to over 8 centimeters. So clearly, there's an endolink. The only question is what type. And you can see that there's separation of the top of the graft from the wall of the aorta with blood flow going around it. You can see it's confirmed on the CTA. And this is a type 1a endolink. This is an example of a 1b endolink that occurs distally at the distal site of the end of the graft. And you can see that the graft ends in the middle of this left common iliac artery aneurysm with blood flow going around it, both on the color doppler as well as on the CT scan. Now type 2 endolinks are due to retrograde flow into the sac from the aortic branch. These are the most common type of endolink. They're usually relatively low blood flow. Many of these are going to resolve spontaneously. And so therefore, they can be safely watched, provided that the aneurysm is not increasing in size or that they don't occur after about two years, in which case, they're generally going to be embolized. And if the feeding vessel is coming anteriorly, as you see in this CINE clip here, you can see it right here, it's going to be due to either the IMA or the accessory renal artery. And if it comes posteriorly, it's going to be due to a lumbar artery. If you get a waveform in the feeding vessel, it typically looks like the waveform in the neck of a pseudoaneurysm, flow going towards the endolink in systole and out during diastole. And if you see that there's continuous forward flow throughout the cardiac cycle, this likely means that it's a complex endolink and there's probably a second one, because there has to be a way for the blood to get out, because if it isn't, it's just going to explode in a very short period of time. Type III endolinks are due to structural failure, break, separation of the module tear in the fabrics. These were uncommon in the past, but now that they're putting in these more complex endolinks with these chimney extensions, the incidence is increasing. These also have a significant risk of rupture, and they must be repaired as well. And what you look for is an actual break in the endograft, as you see here, with blood spurting out directly into the aneurysm sac. Type IV is due to graft porosity. The angiographers see this. Everybody has this, but it is self-limited and disappears. There is controversy as to whether or not the Type V actually exists. This is due to increase in diameter, but you can't find the endolink on any type of imaging. These have to be repaired if the aneurysm is getting bigger. All you can say is the endograft is not working. Usually it's an open repair because you don't know where the endograft leak actually is coming from. And this is an unusual complication. This patient presented with leg pain, and you can see that the left outflow limb here on the color Doppler, as well as on the spectral Doppler, demonstrates no flow. And this is due to thrombosis of the left outflow limb. Now this patient presented with acute back pain, as well as left foot pain, and this is a nice example of aortic dissection. You can see the echogenic intraluminal flap. You can see on the color Doppler flow in the true, as well as the false lumen. And as you all know, aortic dissections begin with an intimal tear, and whether or not you get an intramural hematoma versus a patent false lumen depends upon whether or not there is an exit tear. And the symptoms depend upon whether or not there are involvement of the aortic branches, so you ought to look for that as well. In this particular case, you can see that that echogenic intimal flap extends into the left common iliac artery, and actually it began here on the FAST scan. This is the heart. This is the descending thoracic aorta. It began in the descending thoracic aorta, and you can see this nicely on the CT scan all the way from top to bottom. Often the true lumen is compressed, so velocity may be increased, but typically the waveform looks relatively normal, although the waveform can look extremely abnormal within the false lumen, a very disorganized flow pattern. It is important to look at the branch vessels within the abdomen, the celiac, the SMA, and the renals, because sometimes the dissection flap will extend into one of those branches. And what's interesting, at least in the SMA, and you can get spontaneous dissections in the SMA as well, is that you can see the intimal flap as being a very echogenic linear line as you see here, whether the false lumen is patent or whether it's thrombosed or there's just a mural hematoma. You can recognize that this is a mural hematoma rather than atherosclerosis because it is very homogeneous, it is very hypoechoic, and you don't see a lot of echogenic calcified plaque. And here you can see on the rendered CT this very long segment of very irregular lumen that's very narrowed in this patient with an SMA dissection. And because the lumen is narrowed, velocities are often increased, and these patients can present with pain mimicking mesenteric ischemia. Now when somebody has a dissection and that intimal flap is lifted off the rest of the wall of the aorta, this weakened, or the whatever vessel it is, in this case the SMA, it weakens that vessel wall, and that means that it is more prone to complications such as rupture or development of pseudoaneurysm. So if these branches are not treated prophylactically with a stent, you need to follow them to make sure that complications do not occur. The dissection could extend, it could completely thrombose the vessel, or in a case like this where we got follow-up in a year after a patient had had an SMA dissection, you can see that there's clearly a neural hematoma here, just like the case I showed you before, hypoechoic, very homogeneous, only on one side of the wall, atherosclerosis would probably be on both sides of the lumen, would be more irregular, more heterogeneous with some areas of calcification. And so you can see that neural hematoma, but those of you with eagle eyes will also see that there's a little outpouching here, looks like a little mushroom sitting on top, and this is a pseudoaneurysm, you can see it filling in on the contrast enhanced CTA, and on the rendered image you can see again that little mushroom of the pseudoaneurysm sitting on top of the middle of the SMA. And at this point this does need to be treated with a stent in order to exclude that. Now the more classic appearance of chronic mesenteric ischemia, of course, is narrowing due to atherosclerosis, and remember in order to get symptoms, two of the three mesenteric vessels have to be involved. So here you can see narrowing, focal color aliasing at the origin of both the celiac and the SMA, and you have elevated velocities, 367 in the celiac and 400 in the SMA, so clearly diagnostic of chronic mesenteric ischemia. Remember that if you think a patient has acute mesenteric ischemia, you should not waste time with an ultrasound. This is an emergency. These patients should go directly to CTA, angio, or to surgery. There is controversy as to exactly what criteria that you ought to use. None of the studies are very large. In general, they're single institution. I remember these numbers, frankly, just because they're easy to remember, and I'm friends with the people that wrote the article. Probably not the best scientific recommendation that I can give you. But the bottom line is that I use these as guidelines. I really look for the narrowing, the focal color aliasing, you correlate with symptoms, and so I remember 200 for the celiac and the IMA, 275 for the SMA, but I also try and get a waveform as distantly as I can looking for a tardus parvus configuration, a delay in systolic upstroke, because that will convince me that the elevated velocity, in fact, does indicate a significant stenosis. Once the diagnosis is made, these patients are generally treated with a stent. You can see the stent here in the origin, the SMA. This is a good outcome, fills in, no narrowing, no color aliasing, normal peak systolic velocity. But in this particular case, you can see it's narrowed following stent placement. There's focal color aliasing, velocities increase from 150 up to 800, and you can see there's that distal tardus parvus waveform. Clearly, this is an instant re-stenosis. Now, occasionally, they're going to be treated with a bypass graft. This patient had a celiac to distal SMA bypass graft. Here, you can see the graft here. This looks beautiful. It is widely patent. There is no narrowing. There's no focal color aliasing. In fact, the reason is because there's very low blood flow. The velocities are only 18 in that graft. Well, maybe it's because it's a big graft, but 18 is really low, and that's really a bad sign. It's a pre-occlusive finding, and not surprisingly, when you get to the distal anastomosis, narrowing focal color aliasing velocities of 400, this was a distal anastomotic stenosis. So remember, low velocity in a graft, even if it looks widely patent, is a bad finding. So to summarize, ultrasound is the most effective means of screening for a AAA. Color doppler may be adequate for surveillance following endograft repair. Look for the leak. Look for the increase in diameter. If there are risk factors, though, maybe you want to follow with periodic CT. Questions, contrast-enhanced ultrasound might help. And for aortic dissection, don't forget the branch vessels. And remember that ultrasound is a very good screen for chronic mesenteric ischemia. We're going to cover three different areas. Before you talk about the abnormals, you have to go over the normals. So this is a normal appearance of the hepatic arteries. Good straight up and down upstrokes, persistent diastolic flow, nice little spectral window here for laminar flow. Portal vein is the confluence of the SMV and the splenic vein. It should be continuous antigrade flow. You may have a little bit of phasicity of the flow, but it shouldn't be so pulsatile that it's coming back to baseline. And then you would look to see if there's any turbulent aliasing. Here's a nice example. Hepatic veins, middle and left back vein often join before the IVC. You can have biphasic flow, but it's primarily antigrade. And then again, you should look for absence of turbulence and aliasing. This is your typical normal waveform. And we talk about the different concepts of the waveform in the hepatic veins, the systole of the atrium for A with a transient reversal, ventricular systole at the peak, ventricular overfill, then leads back to return toward baseline after ventricular diastole. This is your ASVD waveforms that you've been hopefully taught in med school. There are variants that can make ultrasound a little bit challenging. You can have a replaced right hepatic artery from the SMA in about 12% and a replaced left hepatic artery from the left gastric. That one's pretty easy to see because you can see it coursing right along that posterior surface of the lateral and medial segment. Normal hepatic Doppler, we also look at the splenic vein and the IVC as you see here. IVC will be biphasic and very pulsatile. Splenic vein is usually fairly monophasic with maybe a little bit of undulation. I know this is a Doppler study talk, so we're going to very briefly talk about how you use Doppler on liver characterization for lesions. There's not a whole lot of value you can look for, whether there's vascularity. But if you really want to know about vascularity of a liver lesion, use microbubbles. If you do detect flow with color in power Doppler, then it's there. If you can't, then you're still not sure if it has some bit of flow. We all know that hemangiomas do have flow, and yet here's a nice example of color Doppler showing the homogeneous echogenic lesion, no Doppler flow shown within it. Any of us who do microbubbles all know that these show quite a bit of flow on the microbubble studies. Focal nodular hyperplasia will often have a spoke wheel pattern from central flow. I've also noticed that you'll see this peripheral rema flow frequently. And then to show you, this is an example of color Doppler. But if you really want to see a good amount of more flow, power Doppler is more sensitive for small amounts of flow. And the new types of microflow imaging are even sort of a super power Doppler to even pick up smaller areas of microvascular flow. Now this is not a benign finding. This is a large infiltrating mass filling most of the liver. And then when you look at the portal vein in this patient, I want you to pay attention to this very low resistance arterialized waveform. It's not just the venous respiratory undulation, but it's actually a pulsatility. So this is arterial flow within tumor and vein. It's no longer called tumor thrombus, but it's actually this is an HCC with tumor in vein by the new LIRADS categorization. Again, if you want to see the small vessels better, you can use power Doppler, and it shows it well. So what is the role in LIRADS for Doppler? It's only for patients at high risk. There really aren't a whole lot of uses unless you're using microbubbles. You can look at the different vessels to see if there's tumor in vein or any occlusion. But mostly, if you're going to try to do LIRADS with ultrasound, microbubbles are the way to go. Here's a patient with gross cirrhosis. We have surface nodularity. We have homogeneous monophasic flow in the hepatic veins. And then this is a patent parumbilical or recanalized umbilical vein, whichever term you want to use. They had dilated main portal vein with reversed flow. And the portal vein was 1.9 centimeters diameter, so this is all consistent with portal hypertension. Anything greater than 13 is abnormal, but we usually don't call it till it's at least 15 to try to increase the accuracy of the findings. If you have reversal of portal venous flow or collaterals, that helps to seal the diagnosis. You can use this. This is not widely used, but as a tumor or inflammatory process takes over the liver, more flow is drawn from the hepatic artery. So its flow goes up. The portal vein flow goes down. So once the hepatic artery end diastolic flow is higher than the portal venous flow, then that can trigger you to think that tumor or inflammation is drawing from the hepatic artery. Portal vein thrombosis can be acute or chronic. In the acute phase, it's going to fill the vein with mildly echogenic material. Chronically, you're going to get stricturing down to the main portal vein and collateral formation. Here's thrombus filling the vessel. Nice, easy to diagnose. It can be a little confusing with Doppler, because here, if you're not paying attention, you'd say, OK, this portal vein is patent if you're not paying attention to the clot along the anterior surface. Over time, though, that will actually stricture down. You're left with this cluster of vessels, which is known as cavernous transformation. Heart transplant evaluation patient. This patient has dilated hepatic veins. And when we look at the main portal vein, there is biphasic flow in this structure. This is a classic testable question in terms of increased right heart pressures. Normal hepatic veins are less than 10 millimeters. We never measure those. Do they look big? Do they look normal size? That's really the extent that we will do. And then we look to see if that resistive index, if you're going to actually try to calculate a portal vein, the peak minus the minus greater than 50%. Anything that's two phasic, though, makes you think of those increased right heart pressures. Now, the opposite end of the spectrum is this, where the hepatic veins are strictured down and not visible on the color Doppler. If you don't believe me, here's a longitudinal. We have the IVC here. And this hepatic vein branch coming, and we lose it right about here. This is on power Doppler. On the transverse, again, we see that patent vessel. But the last centimeter or so is gone. And this is where it should be. So this is a nice example of Bud-Chiari, large vessel occlusive disease with absence of flow in this central portion of the hepatic veins. This is different than small vessel veno-occlusive disease, such as chemotherapy or radiotherapy, where the small branches are involved. And it's not just the central portion near the IVC. All right, so if you have cirrhosis, one of the best treatments is a TIPS shunt. There are a lot of uses for these in the setting of cirrhosis, as we list here. Variceal bleeding, ascites, gastropathy, hydrothorax, Bud-Chiari. A lot of these are done to temporize before the patient can finally get a liver transplant. Does it work? Yes. So it can help with variceal bleeding, even in child's PUClass C patients. And then for intractable ascites, it is better than recurrent large volume paracentesis. Its goal is to reduce the portal hypertension below the 12 millimeters of mercury. The problem is, when you place these metallic stents, we don't do as many of the bare stents anymore. They're usually going to be Gore-Tex or PTFE covered stents. And the reason we use the covered stents is, in the old days, those metallic stents, they really failed pretty quickly. You had an 80% dysfunction rate within two years in those. To be able to use the criteria to evaluate a TIPS, you need to know, well, what did it look like before? So we'll often get a baseline on these, because a percentage of these patients can actually have reversal of flow in the portal vein branches. But some of them, actually in a functional TIPS shunt, never do actually fully reverse. And because of that, you can't say that, OK, anti-grade flow is always bad if it was already anti-grade at the beginning. These are numbers from the literature, but our experience is that this is a lot less common than the 50% or so that they're giving here. Here's an example of a TIPS. We have a velocity of 0.58 within the main portal vein, which is a nice, normal value. Left portal vein is reversed. Right portal vein is reversed. So that's because the TIPS is creating a superhighway going from the main portal vein into the IVC. And therefore, it's sumping the flow away from those portal vein branches. And then within the TIPS itself, we always look at the portal venous side, the mid-stent, and the hepatic venous side. Here we're 150. Here we're 144. And here we're 125. So all of this is a normal study, normal velocities. We like it to be less than, we like it to be within the stent between 190 down to 90 for normal values. And then we want greater than 30 in that main portal vein. The IVC has good velocity, 125. So there's no velocity elevation there. And that's the most common place that we would see a problem. When we're looking at the complications after a stent, the three that I want to really focus on are stenosis, thrombosis, and hepatic encephalopathy. Sometimes the shunt just works too well. And it doesn't filter out enough of the problems or the toxins for the liver. And that can have effects on brain processes. This is an example of a patient with TIPS. And when we put the Doppler on the hepatic venous side, no flow. This is the easiest diagnosis. It's not the most common that we see. But if you have no flow in Doppler, it's a very accurate finding for this diagnosis. Now, stenosis is a little more complicated. Even with the covered stents, we need to keep doing ultrasounds. And that is because up to 25% will still have dysfunction, even with the covered stents. MGH did a study. They compared 41 bare and 40 covered stents. And at 12 months, even the covered stents had a requirement of re-intervention in 38% of the patients. This is an example of an abnormal study. So 0.54 in the main. Left is anti-grade now. So if they were previous retrograde, now the flow is trying to find its way back through those portal vein branches. The right portal vein is still reversed. And then as we go through the stent, we're 124, about 150. And then here's the problem. At the hepatic venous side, we're now at 261 centimeters per second. So we are over that 190 that I told you about. This patient is suspicious for TIPS dysfunction. They're going to go on and have an interventional procedure to evaluate for a stenosis. So in the main portal vein, after a TIPS, the normal velocity is 40 to 43. Once it drops down below 30, we become suspicious. And to me, this is one of the best signs of all. If I have a main portal vein that's less than 30, no matter what the rest of the study shows, I'm still concerned that there's some problem. Also, again, if you had previous reverse flow in the branches and now it's antigrade, that's a problem. We like the criteria from Kanterman and Middleton, 90 to 190. Also, if you use a lower threshold of 50 to 60, that might increase your specificity, as I'll show. A stent gradient within the stent of 50 to 100 from one point to another. And then a change from the past. So if you have a baseline and it drops 40 to 50 or it increases 50 to 60, those are also signs that something's going on with the stent. This is that same baseline study with the reverse normal flow. And then on the follow-up study, we have our flow has dropped to 17.9. Already, I know there's a problem with this shunt. And then we still have the reversal of the left, but that's actually a late finding. We have reversal of the right, but our velocity now is up to 285. So this person is going on for further evaluation to look for the area of narrowing. Again, if you use these combinations, you're going to be in pretty good shape. Less than 30 in the main, 90 to 190 in the stent. Decrease of 40 or increase of 60. And then if you use those lower values, the less than 50 and bring your up to 250, you have a little bit higher positive predictive value. All right, so that's cirrhosis and tips. So hopefully, you're lucky enough that then you can go and have your liver transplant. And hopefully, it's a great surgeon who's doing a good job because these can have a lot of complications. There are five different anastomoses that they're having to place. And we're going to be evaluating the vascular ones frequently. We do a baseline within the first 24, 48 hours. This is just to know how the flow is going, what the velocities are. We document direction. You really want to just show that there is antigrade flow and that there's at least some diastolic flow. We don't need it to be perfect because usually within the first 72 hours, it's going to become better. Here was a patient day one. Good upstroke, but really pretty high resistance flow. Long segment there with no flow at the end of diastole. And then on day four, it's back to a normal appearance. So just give it a little time for the body to accommodate the changes and then get a repeat. If you do have vascular complications, they're usually pretty early in the process. Ultrasound is a great modality for that. And then finding the abnormality early is key to the success. Hepatic artery complications are not real common, but we see them. You want to look and see if there's a low resistance flow, no flow, or a parvus tardus type of process. Focal stenosis is a velocity greater than 200 centimeters per second. If you see these small fluid pockets forming in the liver in the expected region of the bile ducts, you may have gas in them. This is going to be concerning for biliary necrosis because the bile ducts are supplied solely by the hepatic artery. And in this patient, my sonographer said MHA area because she couldn't really find the main hepatic artery. It should be right here. And this was a patient with hepatic artery thrombosis. Doppler is correct in 92% of these, and we can show pretty well. The problem is if you wait too long in a more chronic patient, you can have collaterals which can confuse the diagnosis. Hepatic artery thrombosis is associated with bilomas, hepatic infarcts, and abscesses. Now, if you don't have a thrombosis, you might still have a stenosis. And you look for these types of delayed systolic upstrokes, such as you see here and here. You may have low resistance flow, where RI of less than 0.5 here. So each of these makes me think that if I look more upstream, I may be finding a stenosis. And then on this, as we get where the expected anastomosis would be, we have a velocity of over 200. We're 274. So this is consistent with hepatic artery stenosis. Again, use 200 centimeters per second, post-sonotic turbulent flow, or partus tarvis waveforms downstream. I'll skip on through that. This is another complication that you can have. We have a pocket of anechoic fluid round in the hepatic hilum when we put our Doppler on, which you always should. We've got this rounded structure with a little bit of yin-yang type of flow. And this is a hepatic artery pseudoaneurysm. Occurs after transplant pretty rapidly. May also see it with biopsy if they were too deep, biliary intervention, or infection. Here is a patient where we have the portal vein. And I'll just show you, this has echogenic material filling the portal vein. After transplant, 1% to 6% of patients, often related to surgical technique, misalignment, vessel length, or hypercoagulable state. You are pretty good at finding it if there's no flow. And then you can look for color aliasing at the site of narrowing if there's stenosis. Here is the post-sonotic dilatation in a stenotic patient, not thrombosis of the portal vein. You've got this circular flow. And then as we get into the inflow area, we've got a velocity which is markedly elevated at around 100 centimeters per second. Portal vein stenosis, look for diameter less than 2.5 millimeters, peak velocity in the portal vein of 150, or a 4 to 1 ratio. IVC can have complications because there's an asthmosis there. What I like to do is I look at the Doppler. If it's a monophasic flow, the IVC should be back and forth, up and down. And if it's nice and monophasic like this, I'm concerned about that anastomosis. So we go up to the area where the aliasing is, 263 centimeters per second. This is way too high. This is an area of IVC stenosis at the anastomosis. You can use a 3 or 4 to 1 ratio. Look for that loss of the normal caval phasicity. So in summary, there are a lot of complications that you can look for, not only in a native liver, but in tips. Tips are very valuable techniques to help get these patients onto a transplant and take care of some of the complications, such as varicea bleed and ascites. Understand that the liver transplant is not the end-all, be-all. It does have complications. They can fail. And our job as a sonologist is to try to find those complications as early as you can. Hopefully, you've picked up some of the criteria that I talked about for the tips and for portal vein, hepatic artery stenosis. And this will help keep you out of trouble when you're trying to make the diagnosis because there are different criteria for different vessels. And with that, I thank you for your attention. So in terms of technique, we're going to look at the proximal aorta. That's our inflow vessel. And look at the renal artery. And this is just a reminder. Leslie showed you a nice case here. The renal arteries tend to come off sort of transverse. So if you're scanning, looking for the renal arteries on ultrasound, you may want to be in a coronal plane. And you can see that nicely here, where you can see the right renal artery as well as the left. And you get a much better Doppler angle when you're basically parallel, if you will, to the vessel. You don't have as much angle correction to do because, again, we're screening for things. So we want to actually do angle corrected velocities. We're going to follow the renal artery out to the hilum. And then we're also going to sample the main renal vein. Just a reminder, if you're billing for Doppler in an organ, you have to document inflow as well as outflow vessels. In the parenchyma, I use this basically to look at the perfusion of the organ and also to make sure it's symmetric throughout the kidney. So we're going to sample the segmental arteries, which are right here at the junction of the sinus fat and the medulla, looking at the upper, mid, and lower pole. Basically, again, just to make sure I'm complete, make sure my sonographers don't forget to look at one part or another. Our prior speakers have already mentioned the resistive index, which you guys know the formula for. And in the kidney, normal is greater than 0.5, less than 0.8. Earlier articles let us go up to 0.7. Hopefully, everybody in the room has something less than 0.7. But in older patients, certainly it gets higher, and also in transplants. So our goals are going to be looking, as I said, at vascular abnormalities, as we've been talking about in the rest of the session, but also looking at, do we have a fluid mass or a solid mass? Can we find stones? And looking at some parenchymal injury or compromise, as well as a little bit about biopsy guidance. So I'm going to start first with the easiest thing. Is there flow or no flow? And this is a patient who has no urine output in recovery. He's had a transplant. And you can see here's a knocking waveform. Basically, this vessel, there's nothing going in or coming out of it. There's absolutely no flow in the parenchyma. So this means that there's an arterial inflow problem. This is an arterial thrombosis. We check the inflow vessel, or the providing vessel, which is the iliac artery. You can see that there's flow there. So we know that the problem has to be in the renal artery. And when this patient goes to the OR 30 minutes later and they've taken the clot out, you can see that the transplant is nicely reperfused. And this is really more of a problem in transplants than in natives. In native renal arteries, we're looking mostly at renal artery stenosis. And this affects, actually, a small percent of the population. But it's a fairly common cause for end-stage renal disease. So I don't know about in your institution, but in mine, I seem to have at least two or three of these every day. Somebody who has acute kidney injury, is there a renal artery stenosis? So in young patients, we're more often looking for a cause for hypertension. But that's in my outpatient population, I'll tell you. More often in my elderly inpatient population, I'm looking for atherosclerotic causes. And that is, by far, our most common cause for renal artery stenosis. And it's usually happening at the origin of the vessel. So it's important, again, to get that good view to see the origin. Fibromuscular dysplasia can be anywhere along the vessel. And arteritis is fairly rare. So technique is really important. Again, you have to see the renal artery origins. Unlike some of our other Doppler exams, we're looking for a 60% lesion, not a 70. So when you're correlating back to your CTAs, your MRAs, just keep that in mind. These are the criteria in the literature. Some people use 180. Some people use 200. In my lab, we're using 200. And the sensitivity is very good when you use that threshold. The renal aortic ratio also is very good with a fairly high sensitivity. And if you use both of these together, you do quite well. So I'm just going to show you a couple of cases. This is a 67-year-old woman. She was hypertensive. And they gave her some meds. And then she developed acute kidney injury as her blood pressure improved. So let's just look at the images. Again, we sample starting in the aorta. You can see the velocity here is 78. That's fine. The left renal artery origin, velocity 373. That's way too high. Same thing in the right renal artery, 398. So she has bilateral renal artery stenosis, which you can see nicely here on her MRA, as well as on her CT, which she actually had probably just before they ordered the ultrasound. Did they stent her? Actually, no. They did not stent her. They changed her blood pressure medication. And actually, as they altered her medication and increased her blood pressure back up, her AKI improved. So it isn't always a stent. It's not always a surgical intervention. Sometimes it's medical. In fact, most of the time it's medical. So these direct criteria work pretty well for us. But it is tough to examine the entire artery. So people have asked, is there a problem with that? What about the accessory arteries that were missing? Well, it turns out very rarely is renal artery stenosis isolated to the accessory artery. So you really don't have to worry about that. Again, you're screening for a major problem. And fibromuscular dysplasia, we know we're in trouble there. Often, if you think you're dealing with that, you do need to be looking downstream a little bit at the kidney to see if there's a problem, because you're beyond the origin. So people worried about or tried to develop these indirect criteria. And here they are. Systolic resistive indices and a loss of an early systolic peak. That's this example over here. A delayed acceleration greater than 0.07 seconds. Tardus parvus, slow and low. OK, that's this waveform here. Unfortunately, they didn't turn out to be so reliable, because as people develop hypertension, and again, a lot of our patients that we're screening are these elderly patients, their resistance goes up, and they end up looking a little bit more normal. So I use these indirect criteria for, do I have severe stenosis? Is it really a significant stenosis? Or is there a segmental disease that's involving one part of the kidney and not the other? So I use it as supporting evidence. And let me just show you some examples of where it's useful. So here's a patient with renal artery stenosis, or the question of renal artery stenosis. The aorta is almost 80. And main renal artery here, 162. That's fine, right? And here, we can see distally, sort of in the mid-main renal artery, 60. And I'm just showing the straight color image here. So by number criteria, you would say this is OK, correct? Let me show you downstream. So here's the right kidney for comparison. Here's the left. There's obviously a tardus parvus waveform. So that tells me I've got to go back and check, did I sample in the right place? So what could be the problem here? When you look here, the waveform here in this main renal artery is also tardus parvus. That tells me that the trouble is between this vessel and this vessel. And then you look, and you say, ooh, there's a brewie there. My stenographer didn't sample in the right place. When you send them back to sample in the right place, guess what? There's a big renal artery stenosis. So use it as supporting evidence. If you see it, think about, could there be a more proximal problem? And this patient, you can see she actually has atherosclerotic disease, as well as the small dissection here. And did she get stented? Not right away. Ran medical therapy for three years. Then ultimately, when that failed, she was stented. Just another reminder about using the indirect criteria. Here's a patient with hypertension, poor renal function. Does she have renal artery stenosis? And you can see here she has a sort of a funny-looking aorta. It's a little bit broad here. Velocity is 66, not too bad. But her right kidney, tardus parvus. Her left kidney, not too bad. Main renal artery here, also tardus parvus. Velocity, 14. Way too low. Main renal artery here, velocity 38. These velocities are half of what they were in the aorta. So that should make you think maybe there's a problem here. And let me show you what she had. She had a stent placed. And you can see it's basically occluding, almost occluding, her right renal artery. And the left renal artery isn't too happy either. And she ended up with bilateral infarcts from placement of her stent. But as well as that, she has compromise of the renal artery origins. So very, very severe stenosis can have low velocities. And our moderator, Dr. Scout, likes to say it's not just a chart on the wall. You have to use the numbers in context with what's going on with the patient. So I mentioned stents. Do we use the same criteria for stents? And as it turns out, once you have a stent in, you've actually got the vessel is smaller. So you can expect that the velocity is going to have to go up in a stent. And that is true. So in a stent, a re-stenosis is basically, they don't want to go back in, first of all. So they're not going to go back in until the peak systolic velocity is quite high or ratio is quite high. And this is just a nice example of a severe stenosis that was repaired by a stent and actually is normal post-stent. So this is for native renal arteries. Transplants have their own set of criteria. But peak systolic velocity is what I use in a renal aortic ratio. The intrarenal criteria don't work so well, but I use it to support a more proximal lesion. You may need higher criteria in stents because you've narrowed the vessel, and also because you're looking for a higher grade of stenosis to intervene. And so these are the criteria for post-stent. We're going to switch gears here and look at some more cases where I think renal Doppler is really useful in our kidneys. So this is a 15-year-old child with proteinuria. The gray scale, left kidney is too big compared to the right. Resistive index is normal. Renal veins are patent. So what's missing? And the answer is, when you look at the renal veins, did you see the whole thing? No, we didn't see the whole thing in continuity. Now I will tell you, we did not make this diagnosis prospectively. But when you look carefully, here's the artery. There's where the vein should be, and there's a big clot in that vein. So gray scale sometimes is very helpful when you're looking at Doppler to make sure that you're dealing with the correct thing. In transverse image here, you can see a large clot in this left renal vein as it's crossing under the SMA. You can see it here on the CT as well with a delayed nephrogram. So this is native renal vein thrombosis. Unlike in transplants where it's fairly easy to make the diagnosis, very difficult in the native because the resistive indices are not affected. We don't necessarily have that reverse diastolic flow that we'll see in the transplants. The clot may be incomplete. There can be collaterals forming quickly. So look for waveform changes or absent flow in the affected veins. And again, this is something we did not pick up prospectively. But now, I think I might look for it. When you look at this main renal vein and look at the sample, it's very monophasic here. When you look at it closer to the IVC, it is pulsatile. And so I'd like to see that pulsatility reflected back a little bit more in this vein. So if I see a really abrupt transition, just as Mark was talking about in the portal venous system, you can think about, is there an interruption in between these two areas? Another possibility for using Doppler, you can see this is another young adult with gross hematuria, anemia. And I've already got it marked up for you. Left renal vein, here's the SMA and aorta. And you can see that there's something going on right in here. And when you turn on the color, of course, you can see flow in the left renal vein and a very, very high velocity as this vein passes between the SMA and the aorta. And you all know that this is nutcracker syndrome, right? The left renal vein is trapped between the SMA and the aorta. These patients present with flank pain and hematuria and sometimes scrotinuria. These are the criteria, a fairly high ratio between the renal vein at the stenosis versus the higher velocity or the proximal velocity. And the interesting thing here is that most of these patients don't undergo surgery, if possible. The idea is you wait for them to mature and get some retroperitoneal fat, and that'll open up the space. If that doesn't work, then they'll go in and intervene. So this is my favorite part of the talk, which is where we use color, actually, and spectral Doppler to make other diagnoses besides looking at the main vessels. So for stone disease as well as masses and some other things. So twinkling artifact is really important in my practice. It's a mosaic of colors that occurs behind small, strong reflectors. You can get it with color or power Doppler. And we actually think it's due to surface irregularity with little tiny trapped gas bubbles, so small we can't see them, but they're trapped in the crevices, actually, of the product or the stone or whatever it is we're looking at. So I'll just give you some challenge cases. Can you see the stone here? Now, can you see it? Of course, right? It's right there. All right? And so it provides us quick localization of stones. So we use color in every single renal exam that we do. We're not billing for a Doppler, but we're using color Doppler all the time. So some places where it's very helpful, this patient has large body habitus. I don't see anything here. And when they turn on the color, obviously, they've got stones. Here's a two-millimeter stone. We know it's there from CT. Where is it on ultrasound? Easily seen here. And often, the artifact is quite a bit bigger than the stone it's behind. So how good are we using Twinkle? Well, we're actually pretty good. In symptomatic patients, the Twinkle is 92% true positives, okay? The shadow, if you're using a shadow behind a stone, not as good because we're limited sometimes by the size of the stone. Really tiny stones may not shadow. So again, in symptomatic patients, we do very well. If you put these two together, you can get a combined positive predictive value of 76%. Technique's important. So this is counterintuitive. You would think that to get better technique, you always raise your frequency. Well, it turns out with Twinkling, you actually want to use low frequency and a high scale. So you can see here, the scale's at 25 and the frequency's at 3.6. Here, when we turn the scale up to get rid of the vessels, we take the frequency down. Now, you can see the Twinkling stone. So you want to actually consciously do that in your exams. Again, if you're thinking it's Twinkling, this is obviously Twinkling and not a vessel, but you can confirm it with a spectral tracing. This patient also has medullary nephrocalcinosis. Are there false positives? Yes. If you have an asymptomatic patient, you can get as many as 60% false positives. So be careful because Twinkling is going to occur along your vascular calcifications as well. So if you're seeing Twinkling out in the parenchyma and not in the sinus where you'd expect stones to be, I won't call those stones, okay? Here's just a challenge case for you. This is somebody who is two weeks post renal transplant. It was a living donor, okay? And so here's this Twinkling and you can see that this is obviously noise. Is this a stone? And then here you can see it's sort of in a different location and this is out in the, sort of in the hilum and in near the pelvis. And when you look carefully, what's this? Looks like a pigtail, right? It's a pigtail catheter. So catheters absolutely can trap little bits of air and they can give you Twinkling. So don't be dissuaded. The Twinkling's real. It's just not from a stone and can mimic a stone. Some places, again, to use Twinkling. This is a person with flank pain but there's no dilatation. We get asked to do this all the time from the ER, right? Is there obstruction? And so, yeah, I think I can see this stone. I can see it better here. When I turn on the Twinkling, look what I found. There's the obstructing calculus at the UVJ. It's right there, okay? Not gonna be seen prospectively unless you're really, really looking for it and angling on it. This makes it very rapid to detect it. Some places where you can get trouble with Twinkling, okay? So we mentioned it's gonna happen behind calcifications. This one, this was done at an outlying institution and they turned this on and they said, oh, there's color flow. This is a renal mass. So they sent the patient for a CT, but on CT, again, this is a little bit of calcification at the edge of a renal cyst which they didn't detect. So this is basically, you always wanna turn on the spectral and confirm that actually you do have flow in it and realize your Twinkling is gonna happen behind your strong echoes. Another place where we can use color, this is a question, is this a complex renal cyst? You get these questions all the time, right? You're looking at these patients. And there are a couple of technical errors here. One is that we're not seeing any color in the image. So we should probably get a better grayscale and better color. And when we do that, you can see on grayscale, it begins to look like there's something in there. You turn on the color, and there's obviously flow in this. And this is confirmed with spectral. And this is a cystic RCC. So if I can encourage you to do anything, it's to use, actually, better Doppler to look for cystic versus solid masses. Just remember, tumor vessels are smaller than the main renal artery and those segmental branches. They have slower flow. So adjust your parameters for slow flow and increase your sensitivity by increasing the Doppler frequency if you can, OK? Interventional, we use this for biopsy guidance. And this is just a nice example of why. So this patient had a transplant. They asked for a biopsy. And when you turn on the color before the biopsy, this part of the transplant was dead. So you don't want to biopsy that. That was infarcted, OK? So you want to biopsy where it's living. So we changed the biopsy route. And they biopsied. And they went straight into the hilum. So of course, they traversed some big vessels. And they got a new vessel. And they got an AV fistula, right, which is pretty common after biopsies. They can present with hematuria. But mostly, they're small. And they resolve on their own. And this is the typical waveform arterialization of the venous flow. So again, somebody who routine biopsy, two days later, you see it. But it goes away on its own in four months. Pseudoaneurysms, uncommon. But they can be treated expectantly as well. Here's a patient 11 months later and two years later. It's resolving. Lastly, I just want to talk a little bit about hematomas. You can see this is another nice vessel. And Leslie mentioned this to and fro pattern when you've got a vessel going into a dead end in space. So that's a hematoma. Again, they often resolve on their own. And lastly, hematomas that you can see here, it's important to turn on the color and turn on the spectral. Because you want to diagnose this, which is a page kidney, which can result in hypertension or acute renal failure. Because again, this patient sort of has almost like a cellophane wrap around their kidney. And they cannot perfuse it well. This is absent diastolic flow on the spectral. Where do you think the kidney is here? Looks like it should be here. Surprisingly, we can turn on the color. It's out here. Another page kidney, compressive hematoma evacuated. And with that, I'm going to quit, actually. I just want to remind you, renal Doppler imaging makes a diagnosis for renal artery and stenosis and thrombosis, renal vein stenosis, thrombosis, parenchymal perfusion abnormalities, indeterminate renal masses, stone disease, and pre- and post-biopsy complications. Thank you very much. So, as Leslie says, a lot of people are scared by liver transplant, but it's actually not that bad. So with hepatic transplants, we come really to the treatment of choice for end-stage irreversible liver disease. Annually in the US, unfortunately, about 40,000 people progress to end-stage liver disease and another 2,000 suffer acute liver failure. And then only about 6,000 transplants are performed annually in the US. So you can see there's a real discrepancy between the people who kind of need livers and those that actually get them. Ninety percent of these will be in adults, the rest pediatrics. But even if you're not at a specialized center that does liver transplant, there's a good chance you're going to run into somebody that has a liver transplant. So you really need to know about them. There's basically three flavors of liver transplant. There's what's called the orthotopic liver transplant, where basically it's a whole liver is placed orthotopically in the normal anatomic location of the liver, unlike kidneys where we place them in the groins and the native kidneys are left behind. Then there's also living donor liver transplant and split liver transplantation, which we unfortunately don't have the time to go into. But these are techniques that are really increasing the supply of available livers to donate. So with orthotopic liver transplant, what we basically do is the diseased liver is removed and then the transplanted organ is placed back in its normal anatomic location. So when you're scanning a transplanted liver, it looks like a real liver that normally you would see every day. The technique they do, or one technique they can do, is take the retropatic IVC with the liver from the recipient. This is a cable replacement technique. And this requires putting the patient on venal venous bypass, because now you've interrupted the IVC. And then basically you just divide the portal vein, the hepatic artery, and the common bile duct and take the liver out. So you're kind of left with this situation where you now have this gap where the IVC used to be, and then the vessels here in the porta hepatis are all divided. So what do you do to fix this? Basically very simple. It's just four end-to-end vascular anastomosis and one biliary anastomosis. And if you remember that, that's half the battle, because this is also, as Mark was alluding to, this is where the problems are going to arise. So basically the four end-to-end vascular ones is suprapatic IVC, then they do the infrapatic IVC, then the portal vein, the hepatic artery, and then finally the common bile duct. And since these are end-to-end anastomosis, they're kind of difficult to see exactly where the anastomosis is unless a problem occurs. Having said all that, that's not what we do at our institution. We do something that's called the piggyback technique. So again, not to get confused, what is the piggyback technique? Well, here they actually fillet the liver off the recipient's IVC, so they leave the IVC intact. Now the patient doesn't have to go on venal venous bypass. There's less dissection in the retroperitoneum, less complications. Sometimes it can be a little time-consuming to actually fillet the liver off the IVC, but overall a good situation. And what they do is that common opening into the recipient's IVC, they take where the hepatic veins are coming in and create a common opening. And now the donor liver comes in, and it has its own section of IVC. One end is tied off, and then this end is anastomosed to that common opening we just created. So we have this piggyback situation. So you're going to actually see two vessels on top of each other. And don't get confused. What is this crazy vessel doing where it shouldn't be? All right. And just to show that I'm not lying, we actually see this on ultrasound. So here's the piggyback. You can see the blind ending. And here's the native IVC. So one right on top of the other, and here just with color. And you can actually see that connection they've created between the two at the anastomosis. Now I always used to tell the residents, they would always go, well, you've got this blind ending thing. Why doesn't it thrombose off? And I always used to say, ah, a lot of high flow. Never will happen. Of course, last month it did happen. So we have here actually thrombus in the piggyback. And here's the native IVC. And you can see here on these sinase, there's that thrombus sitting in there. And here's the native down here. And here, nicely, you can see that piggyback with the thrombus and the native IVC adjacent to it. So never say never. All right. Everybody good with that? Now we know how the liver gets in. That's half the battle. And once you know that, then you can see and figure out what goes wrong. And I like to keep things simple in my brain. So basically, I divide it into three areas. There's vascular complications. And they'll be either arterial or venous. There's biliary complications. Or there's things that can go wrong with the liver itself or in the periopatic space. So the vascular complications, first, it's very important to understand the vascular supply to the liver. The hepatocytes receive blood from the portal vein and the hepatic arteries. The bile ducts depend solely on the arterial blood supply. If I was somebody taking a SAM questions, I would probably remember that fact. The peribiliary vascular plexus originates from that hepatic artery and then supplies the bile duct. So this is why everybody goes crazy about the hepatic artery. Because if there's lack of sufficient arterial supply, you're going to get ischemic damage to the bile ducts. They're going to stricture. They're going to leak and create bilomas. They're going to cause cholangitis if everything gets infected. And ultimately, things are going to go real south, and the graft is going to fail. The other thing that can happen is you can get infarcts. And then patient being immunosuppressed, abscesses will form, patient becomes septic, not a good outcome. Or the patient just may go into fulminant hepatic failure. So very, very important. Be crazy. Check the hepatic artery. Make sure everything's good with that. So let's go over what the normal hepatic artery should look like. You should have a nice rapid systolic upstroke. You should have nice continuous diastolic flow. And the acceleration time, time between end diastolic and peak systolic should be 80 milliseconds or less. The RI in the liver transplant, we like to see between 0.5 and 0.8. Again, if I was taking a SAM quiz, I would probably remember those numbers. The RIs, though, and this is just a side, in the first 72 hours, not uncommon for liver transplant to have RIs above 0.8. We don't freak out about that. It usually happens with older donor livers, ones that had a lot of cold ischemic time. Studies have shown they usually do just as well. If it doesn't come back down after 72 hours, then it's cause for concern. The hepatic artery can cause problems. It can thrombose. It can stenose. Or you can get pseudoaneurysms. The thrombosis usually occurs within the first three months. And here's the usual predisposing factors. Or you may have chronic thrombosis or delayed thrombosis due to rejection or sepsis. Treatment-wise, these patients will go on to either thrombectomy if you catch it early enough, arterial reconstruction if you catch it early enough, or unfortunately, retransplantation. The ultrasound findings, basically like any vessel that's thrombosed off, absence of flow by color doppler flow imaging and spectral doppler in the main and intraopatic arteries. However, sometimes collaterals can form. And then in the intraopatics, even though you have no flow in the main, you will get tardus parvus waveforms in the intraopatics. So don't let that fool you. Unfortunately, this can run into areas of false positives because with hypotension, high-grade stenosis, or even hepatic edema, you may see tardus parvus waveforms. But you should still see blood flow in the main hepatic artery in those situations. So one case we had not too long ago. Here the tech is looking, just cannot find any arterial flow, just portal vein. No matter where they look in the expected area of the main hepatic artery, nothing is seen. Patient went to CTA. And here you can see that there's complete thrombosis of the hepatic artery. Patient went to angio. And again, all you're seeing is filling of the splenic. On this arterial phase, already you can see something's going on in the liver, which shows up better here in the portal venous phase. And this already is the bile ducts breaking down. And these are bilomas forming. So already without that arterial supply, they're starting to leak. This patient also had these small collateral vessels that formed coming off the SMA. So actually within the intrapadics, we did see tardus parvus waveforms. Hepatic artery stenosis is the second most common complication. And usually the anastomosis is the most common site. And again, this can unfortunately go on to thrombosis or also bile duct ischemia. Treatments here is generally going to be IR suite, balloon angioplasty, and or stenting. With the ultrasound findings, like in any stenosis, we like to see elevated flow velocities. And the number we use is greater than 200 centimeters per second, turbulent flow. And then tardus parvus waveforms downstream. These tardus parvus waveforms will have a more rounded appearance. They won't show that nice sharp upstroke. And if you measured an RI, which actually you should, it'll generally be below 0.5. The acceleration time, you don't really need to measure it. But it'll be greater than 80 milliseconds. But just a gestalt view of the waveform, you can tell it's a tardus parvus waveform. Nice case of hepatic artery stenosis. The velocities were 255 centimeters per second. And then downstream in the left hepatic artery and right hepatic artery, you can see these tardus parvus kind of rounded waveforms. And that's what we look for to make the diagnosis. And here was the MIP imaging and the shaded surface display imaging of the same patient. And you can see that area of stenosis. And this patient went on to angioplasty and did very well. Another nice hepatic artery stenosis, and this was actually a great pickup by one of our ultrasonographers. She noticed that there was this area of kind of relative narrowing, but very turbulent flow. And then further distally, there was nice laminar flow, and the lumen looked a little bigger. And here, measured the velocities, and it was 278 centimeters per second. Went on to angio, and just like the ultrasound, you can see that exact area of stenosis. And this patient actually went on to stenting, and you can see here the echogenic walls of the stent. All right, on the venous side, the portal vein, hepatic vein, IVC, can all thrombose. And like clot anywhere, you will see no flow. You'll see anechoic or echogenic material, depending on the age of the clot, within the vessel. The portal veins can also stenose. And again, these are usually at the anastomosis. We look for a ratio of 3 to 1 in velocity, pre-anastomotic to anastomotic, or peaks of stolic above 125. IVC can stenose, but now that we do the piggyback technique, that's really not an issue. You don't have that suprapatic and infrapatic anastomoses anymore. So with portal vein thrombosis, again, remember, thrombus can look very anechoic. So this is actually all thrombus. Initially, you may think this is just the area of thrombus, but when you put color on, there is no flow in any of this vessel, and here too. And then with the CT, you can see there's this large amount of thrombus right there in the portal vein. And on the coronal reconstructions, again, that big, huge hunk of clot. With stenosis, this was actually an interesting case of stenosis, because this was actually a huge hematoma in the infrapatic region. Here's the liver up here, and then running through that hematoma was the portal vein. So already, you can see something's going on. There's nice laminar flow down here before the hematoma, but now you've got turbulent flow with this mosaic of colors, and even just looking at it, you can see the narrowing of the diameters. So we kind of marched along there with our spectral Doppler, and here before the hematoma, it jumped up to 144, and then at the beginning of the hematoma, it jumped up to 102, and then kind of in the middle of the hematoma, we're up to 226. So we can see here that the hematoma is causing narrowing and stenosis of that portal vein. All right, so on the biliary side, you can have two different kinds of areas of concern for biliary strictures. You can have what's called anastomotic, and these generally will be right at the area of anastomosis, and everything upstream from this will be dilated. So it'll be dilated common bile duct above the anastomosis, and then dilated intra-hepatic ducts. The more worrisome type of ultrasound finding, and unfortunately, we don't see this well on the ultrasound, is non-anastomotic strictures. And again, these are multiple areas of stricture dilatation. They're intra-hepatic, and why these are very worrisome is these are usually due to hepatic artery insufficiency and compromise. As a matter of fact, I would probably keep in the back of my head for at least 10 minutes, or until you take the quiz. So here we see a typical anastomotic stricture, and here you can see dilatation of the common bile duct, and it kind of comes down to a bird beak, and then we kind of lose it. But with the MRCP, you can see here it's all dilated down to the area of stricture, which is right at the anastomosis, and then regular, normal common bile duct diameter distally, and then dilated intra-hepatics. I've never seen a good case of non-anastomotic strictures by ultrasound, but this patient actually had an ERCP and had all these areas of stricture. So this, we check the hepatic artery. It actually turned out to be okay, but again, hepatic artery stenosis or thrombosis, make sure the hepatic artery is okay if you have non-anastomotic strictures. On the parenchymal side, basically, you can have infarcts of the liver, abscess, hematomas in the liver, and also outside the liver, and then bilomas. With an infarct, you get a nice peripheral, well-demarcated hypoechoic lesion. It's kind of geographic or wedge-shaped, and then on color, you're not going to see any flow. With an abscess, this is going to be a little more thick-walled. Wall may not be as distinct. It's going to be more irregular with kind of thick internal septations. There may be some central hypoecogenicity because of breakdown and purulent material and pus, and then sometimes you may also have hyperemia around it. A biloma usually is anechoic, but this one actually happened to be complex. We thought actually at first this was probably an abscess, and the hallmark of the biloma is they're going to communicate with the biliary system, and again, concern for arterial compromise if you have bilomas. Here with the IR imaging when they went to drain it, you can see that this actually communicated with the biliary system, went all the way down into the comma bile duct, and then into the duodenum. Hematomas look pretty much like hematomas anywhere else on ultrasound. They're going to be hypoechoic, thin, lace-like septations, or they may be filled with low-level hypoechoes. And this on the MR, you can see the transplant of liver here, and this large hematoma as in the ultrasound in an infrapathic location. All right, in conclusion, liver transplant, treatment of choice for end-stage irreversible liver disease. Ultrasound is the initial imaging modality of choice to evaluate the transplant postoperatively for possible complications. Complications again could be vascular, biliary, or parenchymal in nature. And then CT and MRI are valuable adjuncts for further problem solving. Thank you.

ultrasound evaluation

aorta

mesenteric arteries

abdominal aortic aneurysms

AAA diagnosis

aneurysm measurement

endografts

aneurysm rupture risk

preventive screening

endovascular repair

ultrasound diagnosis