I'd like to invite Dr. Ken Chang to the podium. Dr. Chang is the founder of the endohepatology field. It's a privilege to have you here today to tell us where we are today, how we started through a case. And I'm so humbled by also you taking on some of the hands-on, and I know a lot of interest that I saw this morning, and tomorrow, hopefully, as well, we'll keep learning from you. Thank you, and looking forward to your talk, Ken. Thanks so much, Mo. It's a privilege to be here. So as I mentioned to the group this morning, as you're entering into the field of advanced endoscopy and eventual endoscopy, you're joining a family. And I think I'm probably the oldest faculty, so my family is continuing to grow each year, so I'm welcoming the next generation. I just found out today that, so I was talking to Mohammad Atman, and he said, did you know that you trained my mentor, who trained me, and I've trained others in this conference. So some of you may be my grandchildren, and some of you may be my great-great-grandchildren, so it's a pleasure to be here. Except one. That's right. That's right. So I'm going to talk about endohepatology. These are my disclosures. So I have a case, but before going into the case, I wanted to just talk a little bit about EOS shear wave elastography, because it is a new modality, but it's probably in every one of your units, so it's good to understand how it works and what it does. So shear wave, we know that in your EOS transducer, there's a sound wave that goes out and comes back to form the image. With shear wave, there's another wave that's generated by push pulse, and it results in what we call a shear wave. So think of it as a very powerful ultrasound wave that will hit the liver, and when it hits the liver like a water drop hitting the top of the surface of the pond, it'll create a ripple wave that's perpendicular. So if your liver is stiff, that wave travels quickly. If your liver is soft, that wave travels slow. And that's all it is. It's a way of measuring liver stiffness by measuring the speed of propagation of that secondary wave. The difference between transient elastography or FibroScan, it's the same concept except FibroScan does not have any imaging. Shear wave combines imaging and the shear wave, so it's both. So that's the difference. And now with EOS, we have EOS shear wave. So we can measure the shear wave and the stiffness of the liver, right lobe, left lobe, as well as spleen. So I will present a case. This is a 56-year-old female. Referred for EOS liver biopsy, shear wave, and portal pressure gradient measurement. She has a long history of NAPLD and diabetes. She had a liver biopsy 30 years ago in 1983, and it was a very painful experience. And she was told she had fatty liver. She's had chronically elevated liver tests since 2019. An ultrasound in April of 2021 showed hepatomegaly and fatty liver. She is also obese with a BMI of 33. A more recent CT scan of December of 2021 showed a subtle nodular hepatic contour and perisplenic varices, suggestive of possible portal hypertension. She had a percutaneous shear wave elastography in May of 2022, which showed an elasticity of 11.2 kilopascals, consistent with stage four hepatic fibrosis. Her AMA is also positive. Her alkyl phosphatase is normal. Her platelet count is downtrending. It is now 137,000. Her total bilirubin is slightly elevated at 1.2. The ALT is 30, AST is 36. An ultrasound in April of last year showed hepatomegaly and a heterogeneous liver parenchymal. So just when you thought you were going to escape hepatology with interventional endoscopy, it's circling back. So as endohepatologists, you will need to know more about the liver. And of course, the referrals are coming from hepatologists and transplant liver surgeons, but it's really important that we understand what it is that we're doing and why. So for endohepatology, usually the reason for referrals fall into one of two buckets. Either we're not certain what the etiology of the liver disease is, or the other bucket is we know the etiology, but we don't know the stage of the progression of fibrosis to cirrhosis. And sometimes it's both. The etiology is uncertain, and the degree or staging of the disease is uncertain. So in this case, probably it's fatty liver related. But we do have an AMA positive, although alkafos is normal. Could this be PBC? And we know PBC can present with presinusoidal portal hypertension. Could this be seronegative autoimmune? Possibly, but most likely it's from fatty liver. There's a little bit of an alcohol history, but not much. So there is a question of the etiology. And more importantly, there is a question about the severity of the liver disease. Are we stage 1, 2 fibrosis? Are we stage 3, 4 fibrosis? Are we heading towards liver decompensation? And so that becomes important. And when you put the two together, if we can clearly, clearly delineate the etiology, and we can also clearly assess the degree of liver disease, then we are armed with important information to be able to be very intentional in the treatment algorithm. So in this case, if we confirm that this is MASH, and we show, say, that there's stage 3 fibrosis, and we show that the portal pressure is already elevated, that puts us in solid ground to say, OK, it's not just diet and exercise and see you in three or six months. We have to be much, much more aggressive, possibly endoscopic sleeve gastroplasty. So it does become important. And the selling point of endohepatology is that, potentially, in one procedure in certain of these patients, we can solve all of those questions. We can solve the etiology question. We can solve the progression question. And if they're coming in for an endoscopy anyway to rule out varices, so the one-stop shop where you include EGD, EUS, shear wave, portal pressure gradient measurement, and liver biopsy all in one procedure, we find that extremely gratifying. And also, our hepatologists really appreciate the efficiency that we can provide. The world is not all accepting of endohep. There are a lot of centers where this is emerging. And there are still a lot of centers where people are kind of skeptical that this is going to be a real thing. So it's quite variable. But this case demonstrates the power of endohepatology. So I will move on now to the actual case. So I'm going to start with imaging. So we can look at the surface here. A little bit uneven. So immediately within seconds of imaging the liver, you're going to look at the liver surface for any unevenness. You're going to look at the edge of the liver to see if it's sharp or blunted. And then here, I'm doing a little bit of a liver palpation. So liver palpation just means you big knob up against the left lobe, and you see how much of the liver will indent as you push into it. I've been doing this for decades, and I taught it to Marvin Yu at the Brigham. He ran with it. And there's a paper this month in GIE that's entitled EUS-guided liver palpation. And they showed that it's better than Fibroscan. So very interesting, a very low-tech, very low-cost procedure. You just indent the liver, and you measure the distance of the indentation. If it's 3.5 millimeters or less, almost 100% stage 3 for cirrhosis. If it's greater than 4 millimeters, it's almost 100% not advanced disease. So anyway, take a look at that, but it's interesting that even liver palpation can be useful. And it has this mottled appearance. Okay, left lobe, 13.4. So you will—oh, sorry. You will be doing this tomorrow in our endohepatology station. You'll be practicing shear wave, so I don't have to go into great detail. So the other thing that we do is we assess the spleen, measure the size. And then we can also do shear wave of the spleen. There we go. All right, so why bother doing shear wave of the spleen? Well, it turns out that measuring liver stiffness can be confounded by inflammation or fat. And so you can get an artificially high number because of inflammation. But the spleen, if the spleen is stiff, there's nothing that could cause that other than sarcoidosis or something rare. So if the spleen is stiff, that's almost always related to portal hypertension. So while Fibroscan can only look at right lobe, we can go right lobe, left lobe, and spleen. Spleen is 35. So 35 is elevated. And then here we're going to the other lobe. So left lobe is 13, right lobe is 16. That variability is actually quite common between the two lobes. So now we're ready to do portal pressure measurement, and then it becomes important to identify the relevant vascular structures within the liver. In here, we're assessing the four phases of the pulse wave that is characteristic for the hepatic vein. So this is the left hepatic vein. And that is the left portal vein. So after identifying the vessels, now we're going to target it for portal pressure measurement. And so here we're using a 25-gauge needle. And the technique is very straightforward. You're going to just put the needle through the stomach wall, into some liver, and into the vessel. All righty, there's my needle. So this technique is called the through-and-through technique. The vessel is smallish. If you approach it slowly and gently, the vessel will collapse, and it's hard to get the needle into the middle of the vessel. But if you just go through both walls, and then you retract the needle, it opens the vessel up, and you can see the tip of the needle slide into the middle of the vessel very easily. Went through and through. I'm going to pull it back nice and slow now. And I want the needle just to fall into the vessel in retrograde. So once we're in the vessel, we just flush it with some dilute heparin, saline, and then we wait for the pressure gauge to equilibrate. And here it's equilibrating to five. And then we flush it again, and let it equilibrate. It takes about 30 seconds, and we get five, five, and five. So three measurements, and they're all precise and identical, and that's very typical of what we see. I'm going to take the needle back now. So now we're targeting the left portal vein. The needle goes in. Again, technically not difficult to target. And we flush the needle, and we get a pressure of 11. And the second measurement is 11, third measurement is 11. So 11 minus 5 is 6. The gradient is 6 millimeters of mercury. It's portal hypertension. So you've diagnosed this patient as having portal hypertension. Not clinically significant, because you need 10, 11, 12 before you see varices, before you see portal hypertensive gastropathy, before you see ascites. But they're already on that slippery slope towards decompensation in the near future. So I'm going to show you now the biopsy technique. So before I show you the video, I just want to show you, because a lot of people ask me, how do you get such nice liver biopsy? And this is after decades of refinement. When I use the 19-gauge Fancy needle, this is a super, super sharp needle. And so I prime it with heparin. The heparin never touches the patient. The heparin just stays in the needle. And then what I do is, on my first pass, first actuation, when I'm throwing the needle into the liver parenchyma, I want the needle to cut on its own. So I will take the syringe off the back end. So in other words, the front door is open to let the liver in. The back door is open to let the heparin out. Because if I close the back door and I jam it, it doesn't come through, because it's already loaded with fluid. So I open the back door and the front door. And so the needle is sharp. It's stable. With the first actuation, no suction is needed. Let the needle cut on its own. Suction may cause fragmentation. If you add suction on top of the sharp needle, you'll fragment the liver on the first pass. The needle is primed, but take the syringe and stopcock off before you push. The actuation, after you've actuated, then you put your syringe on, turn on suction only for two seconds, and then turn it off. And I'm going to show you the video now of how we do the first, the second, and the third actuation. I'm going to recheck my distance. Okay, so I'm checking my distance. I'm in the right lobe. And I'm going to get ready to do my first actuation. 40 cc syringe that's already, the suction is already turned on and the stopcock is already closed. But when I make the first actuation. So I'm going to now take the syringe off. So here's my tech Jay, he's going to take it off. And I'm going to then get ready to fire and fire. So this is really fast. You're going to use your elbow and your wrist and go 90 miles an hour if you can, because you're driving that sharp needle and cutting liver very, very quickly. So then the actuation is complete. Now I'm going to put on the syringe, turn on the suction for two seconds. Okay, put it on. Okay, I'm going to suction on. Two seconds suction off. Okay, so now I'm going to bring the needle back. I don't want suction to be on when I'm retracting the needle, it's just going to suck in all that blood. No, no, no, no use in that. So now I'm ready. I'm at this kind of ready position. And I'm ready for my second actuation, the needle does not come out of the liver, you only made one hole in the liver, but you're doing multiple actuations. So now I just change the angle of trajectory. And then I'm going to fire my second actuation. But this time, I'm going to add suction, I'm going to add suction just before I actuate. Why? Because in the needle is already specimen and blood. And now I need suction to move the first specimen up as I let the second specimen in. So do you see the difference between the first actuation and the second? And then I do that again for the third actuation. So three actuations, number two and three, I use dynamic suction. So this is the second, and this is the third actuation. Now I'm ready to pull the needle out. But obviously, before taking the needle out, I turn on eflow to make sure there's no blood flow in the needle track. And I usually wait a couple of minutes. So you don't want to take the needle out while there's flow in the needle track, because obviously then it'll bleed. So technically, it's not bleeding. And then once the needle track stops, then you can take out the specimen. So this is the specimen. It's about 20 centimeters long. And we're going to take a look at the histology. This is left lobe. This is four out of four cirrhosis, right lobe, super long, greater than 20 portal tracks. And this, again, is four out of four cirrhosis. So finally, for safety, if you encounter the flow continuing despite waiting three minutes, this is what you can do. So here I'm doing, I'm about to, I did my three actuations. I want to take the needle out, but the flow is just continuing. So now, again, you don't want to take the needle out. It's very simple what you need to do. Take the stylet, put it back in the back of the needle, push the stylet one third to one half of the way in. And that will give the patient back the last third that came in the needle. That last third is mostly clot. It's already clotted in the needle. And you're essentially delivering a blood patch. So you'll see here in the video, this is the blood patch. Half of the needle. And so now I can safely pull the needle back, and the needle track has stopped. And the needle can safely be pulled back. So thank you for your attention, and I think we'll have the discussions later. Thank you.

endohepatology

liver stiffness

EOS shear wave elastography

liver biopsy

NAFLD

Dr. Ken Chang