Lobar Redistribution | Diffuse Liver Diseases - Part 1a
Lobar Redistribution | Diffuse Liver Diseases - Part 1a
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Another sign that we can see, indirectly, of cirrhosis is lobar redistribution. With cirrhosis, the lateral segment of the left lobe of the liver enlarges, that is segments 2 and 3, and also the caudate lobe enlarges. And with this enlargement, the tip of the left lobe approaches the spleen. The atrophy of the medial segment of the

liver, that is segments 4a and b, will lead to widening of the gallbladder fossa and also widening of the fossa for falciform ligament, and the falciform ligament venosum/g. Also there is atrophy of the right lobe of the liver, that is segments 5, 6, 7, and 8. So in this patient we can see that there is parenchymal

This is another patient with heterotaxy syndrome. In this patient we can see a midline liver which is generally located more on the left side, the heart is also on the left side. When we look at the axial images we can see that the spleen and the liver are both left sided, okay. But also, there are bilateral adrenal masses which

are high signal intensity on T2, and which demonstrate fluid-full levels because of hemorrhage. So this patient actually has two different syndromes. Left Sided Liver, Spleen, Heart, and Stomach with rotational abnormalities of the bowel, which I didn't show you. And these are consistent with situs ambiguous, and then bilateral pheochromocytomas.

The patient also had a known medullary thyroid carcinoma, and so they also have multiple endocrine neoplasia type II. When we see

So this case is used to illustrate some problem that we all have. So here's HCC in the right hepatic lobe. It's actually a cyst next to it which is a really good landmark. This is a 53 year old male and we got in and we do this ablation.

You can see we kinda undercut the tumor in this case. Rather than doing the wedge we actually kind of undercut it from one side but it works just as well, and here we are at the end of the ablation everything looks good. You'll see by the way that there's a very consistent theme in how I do my ablation, you'll see five minutes at 65 watts for almost every

patient. And there's a lot of reasons for that but probably the most important one is I'm kind of a simple guy and if I start messing around with a whole bunch of different settings and change in the way I do things then I find it difficult for me to predict what I'm gonna get. I just think the simple you keep it the more consistent you make

it the more likely you are to get consistent reproduce-able results. So we mess around a lot in the lab in the pigs, working on their livers and kidneys but when I'm working on a patient I wanna make sure I have a predictable consistent result that's gonna give them a great outcome. And so five minutes, 65 watts I use pretty routinely. The only alteration

I'll make to that, is number one, if I'm getting too big of an ablation I'm gonna injure something, I'll turn down the power or number two if I'm not quite covering as much as I want I'll continue the ablation for more time and that gives me a little bit larger ablation zone.

But once again it depends upon your equipment that you use. So here we are afterwards everything looks good on the ultrasound, and the question comes up do we have a complete ablation. I told you earlier that we should do immediate assessments and determine if we've got a complete ablation. So how do we know if we've got a complete ablation?

Well we usually do something like measure from a landmark and try to figure out if the tumor is centered there, things like that, how big our ablation zone is etc. This looks really good but are we sure that that's ablated and that's always a challenge for each and everyone of us as we go through these cases.

I wish it was simple and straightforward but it's often not. The good news is, is there's things coming to help and it's technology driven and every manufacturer pretty much has something like this in the works, this is one of the systems that I'm familiar with and as you can see what they allow you to do,

I don't know if you can tell, there's a little red circle in the center of that and that's the tumor pre-ablation and then the green is the overlaid ablation. And they do a registration technique to make sure that those line up and they make sure you've got a complete ablation.

So there's a lot of software coming down the pipe right now. Cryoablation has one that not only does this, but also shows you a planning before hand predictive of what they think the ablation zone would be. I haven't actually worked with it so I don't know how accurate it is but those kind of things are definitely gonna evolve and they are gonna make our jobs actually a lot easier to be honest with you.

that liver is slightly lobulated, and the lateral segment left lobe is enlarged and approaching the

spleen, which itself is a little bit enlarged. This patient had two liver diseases, and over a course of three years, the developed accelerated cirrhosis. So as I press the button here you're going to see the changes in the liver over the course of three years. You can see that the liver is shrinking overall, but also that the distance between the lateral segment of the left

lobe and the right lobe has increased. Ansd this is due to the continuing atrophy of the medial segment of the left lobe, that is, segments for 4a and b. Segment 4b, in particular, shrinks significantly during cirrhosis. This patient's synthetic liver function also significantly worsened during the three year period. [BLANK_AUDIO] The diagnosis

we see processes that look very aggressive, but in fact are quite

benign. In this patient on T2-weighted MR, we can see that there are numerous cystic lesions that are following the portal triads and branching out. These are peri-biliary cysts, and we can see them most often in patients who have hepatic cirrhosis. When they're very prominent such as this patient the

diagnosis is a little more apparent, but they can be relatively mild, as in this patient, and especially on CT scan, they can be mistaken for hepatic malignancy. So the important thing about peri-biliary cysts is to identify them and to ensure that they're not mistaken for malignancy. This is a 22-year-old female with chronic epigastric

of cirrhosis can be made on ultrasound by looking at the direct

signs that is, surface nodularity and parenchymal nodularity. Surface nodularity is best picked up by using a liner probe, parenchymal nodularity becomes apparent in advance cirrhosis due to fibrous bands that make the nodules more apparent. Heterogeneity of the echotexture is not a great sign in ultrasound because it has a lot of inter and intra observer

variability. The increasing stiffness of the liver makes the hepatic veins smaller, and also increases the pressure leading to portal hypertension. Therefore, the portal vein caliber can increase in size. There are also extrahepatic signs of portal hypertension such as multiple varices, and splenomegaly.

this was actually a trainee case. This was a woman with a very small left hepatic lobe tumor, some

variant anatomy with a gastrohepatic trunk. You can see TACE was prescribed and you can see the gastric branches on the left hepatic trunk arteriogram. And actually this was late in the year, the trainee was by himself in the case and

he mistook the gastric fundal blush as tumor, didn't notice the left draining left gastric vein. Usually you would anticipate from liver to see hepatic venous drainage and began to get his catheter in a more selective position and give chemotherapy to the gastric fundus.

At that point I came by the room said, whoa! Let's stop, we re-positioned the catheter, stopped injecting the chemotherapy, advanced the catheter, saw the true enhancing tumor and applied treatment,

nice chemotherapy uptake. And in this case the patient actually did pretty nicely, no abdominal pain, nausea, vomiting, tolerated oral intake, after TACE without issue and she was discharged home. We added a PPI for her but she remained asymptomatic,

and a nice result at one month.>> So was whoa the only thing that you actually said when you- >> [LAUGH] I like to take it easy on these guys

yeah. >> [INAUDIBLE] >> Sometimes it's nice to know you can get away with I guess right? >> [INAUDIBLE] That was the procedure that had happened to the patient in the past for that patient. So that's a good point perhaps the patient had recruited

vessels from the hepatic circulation to supply that previously embolized location. So that's an astute observation there. >> Why are you treating those [INAUDIBLE] >> The question is why are we even treating those with TACE, can

you->> [INAUDIBLE] >> The hepatic tumor in case one? Either one of them, I guess that's an institutional and personal preference and there's a lot of options for us. At our institution we use all three forms of therapy but in these

particular cases. The operator had selected conventional TACE which I think is appropriate for parenchymal lesions like we saw in those two cases. Yeah question >> [INAUDIBLE] >> Well that-

>> [INAUDIBLE] >> We won't get too lost in the weeds on answering those types of questions but nonetheless, patient did pretty well. I wanna briefly overview non-target embolization, incidence is pretty low. It can span from anything from colocentesis,

pancreatitis, all sort of lesions, and the severity can be related to the embolic load size and collateral perfusion. We see high attenuation chemotherapy on CT, might not be able to see it on MR.

And we talked about some avoidance techniques, careful angiographic review, selective therapy, cone beam CT for real time therapeutic monitoring. You can embolize vessels or use cold packs to avoid non-target to superficial structures and consider vasodilation of treatment beds with things like

Nitroglycerine and then there's some specialty catheters obviously. For management I think subclinical cases can be observed. We use PPIs in our second case to help prevent EGI symptoms and symptomatic improvement to improve patient comfort and then escalation is needed.

[MUSIC] Hello I'm Korosh Khalili. I'm an associate professor at the University of Toronto. I also work here at Toronto General Hospital, thank you for joining me for a two-part talk on diffuse diseases of the liver. In this talk, I'm going to be talking about the cirrhotic liver, the fatty

liver, the mutant liver, the congested and infected livers, the shunted and the infiltrated livers, and the malignant liver, and the bizarre liver. [BLANK_AUDIO] This patient has cirrhosis. And you can see

Here is another one. This is an interesting case, they have a large hepatic hemangioma. It's progressed in size and it's giving him back pain.

A young man and he's kind of a little bit desperate at these point actually, so we were asked to take a look at him. So here is the tumor about 14 by 12 by 10 cm or so. We think this is a good case for ablation, how many would take this case on? Hands up , I see my colleague and maybe one or two others.

So the short answer is, I actually think that these kinda cases are probably the best cases we can have for ablation, benign tumors are an excellent target, both from the stent point,

it's an excellent option for the patient, and number two is an excellent growth opportunity for what we do. So, it is a completely untapped territory as far as I can tell. This is the procedure I did, I kinda split the tumor into two separate

portions, one is a superior margin and one is an inferior margin. And I took it and I did three burns in each location, placing the deep margin burns, pulled back burns, pull back burn and then pull them out.

In the end, let's see here, here's what it looked like, so you can tell by looking at it there's probably some enhancement around the periphery. So I probably didn't get a complete ablation, probably 90% of the

volume of the tumor, but that's more than adequate actually in this case. And the reason is this, if you look at this, this is a movie showing you tissue contraction especially with microwave,

tissue contraption is very dramatic, so if you watch this you can actually see the tissues getting pulled in, those green markers mark where those markers were at the start of the tumor during ablation, and you can see them getting sucked towards the center.

Almost all the contraction occurs in the short access which is one reason that our short access of ablation zone is shorter than the long access but, you can see, very significant tissue contraction. And the end result of that in this case, is you can see there is

my pre-ablation volume, and here is my post, and my arrow is not showing up. There it is, maybe. You can see,

so it's about half of the volume, immediately after the procedure and now I've had the patient gotten immediate pain relief, because he was getting pain from mass effect not from the tumor itself, other than the mass effect.

So this is a very important thing when it comes treating benign tumors. Remember, our goals of treatment are very different. We're trying to devascularize a tumor in the case of adenoma in particular, to decrease the risk of hemorrhage, we're trying to

decrease mass effect in this kind of malignant transformation risks associated with adenomas, but remember you don't have to get every single cell. So even if it's a big tumor like that it's not my goal to kill the entire tumor with a margin it's my goal to improve the patient's

symptoms, and quality of life. And they also seem to ablate easier than malignant tumors probably somewhat because the perfusion may be a little bit less. And so we can even target very large tumors. That's when the larger ones we've done, but we've done many tumors in similar size. So this really as a less invasive answer to a minor problem,

if you are a young person would you want a major liver surgery or would you want just a simple ablation? Hepatic adenomas are very easy to do too, here's a four and a half centimeter hepatic adenoma. You can see we kinda have nice ablation zoen.

These patients go back to work within days, versus the surgery where it tends to be long recovery. Here's kinda the cautionary tale. A young medical student, he wanted to be a surgeon and I think as

a result, he was kind of taking down the pathway of getting a hemihepatectomy. We wanted to do an embolization followed by ablation. And here is what happened to him. He actually needed a re-exploration for high grade bowel obstruction, and we all know that he's kind of headed fast in trouble to the

rest of his life probably related to adhesions and adhesive disease and bowel obstruction. So realistically, we could have done in a merry minimally invasive way and instead, he's got a major surgery. Works for hepatic cyst too. We place the antennas and we drain the cyst around the antennas

and then we do a relatively short burst of ablation, and we can get excellent result. Here is the cyst before and the cyst after. Six months later, you can see is about 10% of the volume of the cyst left.

The patient was completely asymptomatic. Here is another case.

fatty infiltration of the liver. This is a patient that presented to us with no history of liver disease. On ultrasound exam we can see that there are numerous, well defined, echogenic foci distributed throughout the liver. These don't cause any kind of

distortion of the hepatic vasculature, and there is no change in size of the liver. And so this is a typical appearance for nodular fatty infiltration. This can be proven, in this patient, by just doing a follow up scan. And very commonly, either it will resolve or in his case we could see that diffused fatty infiltration of the liver appeared. [BLANK_AUDIO] On CT scanning, nodular fatty infiltration can

sometimes appear more sinister. We can see nodular fatty infiltration, especially in patients who are undergoing chemotherapy, and this pattern can appear like the patient's primary disease. To prove that this is fat infiltration and not malignant disease, MR would be the best modality. And in this patient, we can see that we performed a subtraction image between in and outer

phase gradient echo dual echo T1-weighted images. And so, anything that has any signal or bright within the liver has fat within it. So in the patient we can see that, not only there is diffused fatty infiltration in liver, but there are also multiple small increased areas of signal that are consistent with the nodular fatty infiltration. There are multiple different patterns of fatty infiltration within

the liver. Fatty infiltration can be diffused, as in this patient, where we can see, despite the contrast enhancement, the overall attenuation of liver is quite low and approaching that of water. Fat infiltration can also be lobar or lobulated angiographic, as in this patient. We can also get more well-defined geographic areas within the liver, and again, this is

a patient who's been on chemotherapy. And so this pattern of appearance can mimic malignant infiltration. We can show that this is fat infiltration by either doing MR or ultrasound, and here you can see on the patient's ultrasound, very easily, we can identify this geographic appearance to the fat in that region. Generally, infiltrative/g malignant/g disease will appear at hypoechoic to the [INAUDIBLE] parenchyma whereas,

the fat will appear as hyperechoic. In this patient we can see that there is subcapsular fatty infiltration, and this is really as a response to intraperitoneal insulin that was given in patients with peritoneal dialysis. [BLANK_AUDIO]

So that brings me to the end of my cases.

My kinda conclusions you can see here really I think you had to strongly consider microwave over RF. I think you really can accomplish everything you can with RF and more. And I like to keep things simple, so I try to minimize how much

I go between different systems. Maybe you do enough cases and are comfortable enough with a bunch of systems that you can do that, but I don't feel comfortable doing that myself. I really think you shouldn't use ultrasound for guidance and

monitoring. I really think that the immediate assessment is important if you can do it. You can either use ultrasound or CT. You can do the contrast enhanced study. We use ultrasound particularly in patients with renal failure for

doing that assessment but most times we use CT. Becoming familiar with hydrodissection techniques is really critical if you're gonna do ablation. About a third of our cases that we do involve hydrodissection. We probably do a little bit more of a complex patient case load than most people but you really have to do it if you're

going to do it well. Ethanol for central tumors, or preductal tumors more accurately, I think is a good idea and really does, I think, still play a role even in this day and age.

You really should think about combining with intra-arterial therapy for larger or infiltrated tumors in HCC and remember the ablation near the gall bladder and heart is safe and the software packages that are gonna do both planning and post ablation assessment are gonna make our lives much easier. Thank you very much.

So these complications that we're talking about as well, with really good technique, with employing multiple sort of adjuvant things

to how you do your embolization can actually be reduced. So here's a patient that was embolized prior to my working at the University of Colorado. It's a 43 year old female on chemo for metastatic rectal cancer. She has to keep getting her chemo cancelled because she keep's showing up with her platelets too low, they can't get them up despite transfusing her with platelets and so they have

to keep cancelling chemo appointments and so she asked is there anything we can do and one of our oncologist sent the patient to us. This patient was embolized by one of my partners. She was referred for partial embolization, you can see she has quite a large spleen, it was 18 centimeters at the time and that was probably due to a combination

of lots of chemo and previous selective internal radiation therapy and this was sort of in the time before people were doing lobar to try to decrease the portal hypertension caused by cert. And then so this is sort of the angiogram that was done, she isolated the lower pole, she embolized that whole lower pole with about

half a vile of beads a one to three of three to five hundreds and then she took the rest of it and just kinda flashed it into the main splenic artery. And she ended up getting a decent result from the stand point of the amount of spleen that was devascularized you can see what it looked

like at one week and then following ten months. The problem is this patient spent two weeks in the hospital had a couple of parecentesis, a couple of thoracentesis and was on a dilaudid PCA for a week and so not exactly our favorite thing to ever happen but that was kinda how it worked.

She then came back ten months later Later and this is images from her ultra sound of the devascularized portion of the spleen in the associated ascites adjacent to it. And prior to this embolization, her platelets were 39 immediately following they went up to 155,

but she actually recurred a year later which you can kind of expect if you had actually, done the volumes on the spleen. She actually took about 40% of the spleen and most of the data says if you don't take at least 50% you are going to recur with respect to the thrombocytopenia.

Platelets 89 at this time referred for another splenic embo. So I brought her to the suite and I did it a little bit different than my partner to try to reduce these complications. This is the hematology patient who basically has a normal liver function and so I can do a lot of tricks in this patient that I

can't do in my liver patients. In particular I gave her inter arterial toradol right before I started the procedure. I started the steroid taper with the first dose given in the holding room prior to starting the procedure and then I did a seven day steroid taper, I gave two weeks of antibiotics and then for patients who can get nonsteroidal anti-inflammatories, I give three days

of burst NSAIDs so I give 800 tid of Ibuprofen. And it's amazing the difference that that makes relative to what you normally see with these splenic embo patients and nonsteroidals just they work better in these patients, I don't know why but they do. And so I basically did an angiogram just like that, picked on another

lower pole vessel, embolized it to stasis with 500 to 700 micron particles cuz again the pain can be related to the size of the particles you use. The smaller you use the more likely you are to have pain but you don't want to use too big a particle because, There was a nice study published in the pre transplant literature

from Europe, which demonstrated that if you use particles larger than 800, you tended to get more recurrence of the thrombocytopenia, because they develop intra-splenic collaterals. And so this patient was put on a PCA overnight, didn't need the PCA in the morning.

Went home with her non steroidals, and actually came back and saw me a month later in clinic, and was just fine. And then she actually did fine until later. You can actually see this a lot colon cancer that's in her liver.

So, she actually died five months following or four months following the procedure? Yeah. Four months following the procedure platelets 255 immediately following the procedure, ann 155 at the time of her death. Probably in part due to her spleen but also because she was getting

chemo at the time, right up to the point of her death.

typically if it's isolated to a hemi brain stem, you're going to get contralateral cranial nerve involvement and then contralateral body involvement. Here on this lateral medullary, you can see you've involved the spinal thalamic tract and I'll show you why but they end up having basically decreased pain and temperature on the contralateral body. And then all these other findings are

all ipsilateral and that's because they're involving the brain stem nucleus. And I'll go into that further into the talk here. Then the basilar is formed after the combination of verts coming together. They then travel up, the basilar's riding on the surface of the pons, sending in pontine perforators. It then gets to the base of the brain and then basically splits into the PCAs.

There's also several other arteries that feed the cerebellum coming off there. The AICA and superior cerebellar. And then basically the PCAs then feed the occipital lobe. Looking at the posterior circulation with respect to the cerebellar arteries, we've already talked a little bit about the PICA, which basically comes off of the verts before they come together to form the basilar. The AICA

and the superior cerebellar actually come off of the basilar artery and then these feed different portions of the cerebellum as you can see on the slide here. The superior does what it's described, the superior cerebellum. PICA we know gets the inferior portion, and then the medial portion of the cerebellum is supplied by AICA. Remember, strokes in the cerebellum present ipsilaterally, and

that's because of a double cross, so to speak, of the various tracts. So if somebody has a right cerebellar stroke, they are going to have right body control problems. If somebody has a left cerebellar stroke, they have left body control problems. That's an important message to take away. Now cerebellar strokes, because of the location of the cerebellum and the fact that it's in the posterior fossa

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