So, next speaker, I'm very honored to be introducing Dr. Peter Dragunov, who is a professor of medicine and also director of advanced endoscopy at University of Florida. Dr. Dragunov is also the immediate past chair for our advanced endoscopy committee. Very thrilled to have him here, and he's going to be talking about a third-space endoscopy video case presentation. Thank you, Sai. Actually, I didn't read the fine print. My case is ERCP-related, but hopefully still will be educational. And, Kent, I have a news for you. You probably have great-grandchildren, because when I was learning EOS, there was this instructional video that Kent put together, and it actually came on a floppy disk, and I liked it so much. When I bought a new computer that didn't have a floppy, I was out of luck, because I was using it for our fellows. But it was awesome material, and so Kent has contributed in a major way, and you see why. I mean, it's a fantastic way to present the information in an accessible way. I'm going to go very low-tech. I don't have a single video, actually, in my presentation. Let me see whether I can figure out how to work this. Okay. My case, 54-year-old female, jaundice, fatigue, nausea, and some vomiting for about a month. And, basically, everything else is negative. No pain, no recent medications, no sick contacts, no blood transfusions, no drugs. Basically, we have a patient with painless jaundice. And here are the labs. You see a sodium of 114, and potassium of 3.2. Chloride is also low. There is no gap, and some kidney dysfunction. So, certainly, sodium being so low gives you a pause. And the bilirubin is 26, with highly abnormal alkaline phosphatase and some elevation of the transaminases, albumin 2.6, total protein 6.7. Lipase normal, lactate slightly elevated, mild elevation of the INR. Serum osmolality is 285. Cholesterol, very high. And triglycerides, actually, are normal. Most of the cholesterol is LDL cholesterol. And, actually, I said I don't have a video, but I do have a video. This is the video. It's the CT scan. Pay attention to the gallbladder. The bile ducts are dilated intrahepatically, and now the gallbladder comes into view. And there is a mass in the gallbladder. Certainly looks suspicious. Axial stent. Axial stent? Of what? So, it looks like gallbladder cancer, obstructing the biliary tree. That appears to be the working diagnosis. And ERCPs were requested to decompress the bladder. And anesthesia said, no way, Jose. The sodium is 114. We will not put this patient under anesthesia until you correct the sodium. And my question to you is what you will do next. And I would really appreciate if you give me some feedback. If you want to order additional tests, which tests that will be, look on physical exam for edematous state. As you know, some of the most common causes of hyponatremia are associated with edema. Sclerosis and nephrotic syndrome being the two most common ones. Initiate oral fluid restriction. Common therapy for hyponatremia. Give 3% saline. Call nephrology consult. Or tell the anesthesiologist they don't know what the hell they are talking about. And tell them to proceed with the ERCP. That is correct. Any other suggestions that you want to do here? Anyone wants to run any additional tests? Measure of smallity. It was already measured. I gave you. It was 25. But that is absolutely the correct answer. So you are twice given us basically what we need to do here. So the correct answer is the last one. Tell the anesthesiologist they don't know what they are talking about. And I told them so not exactly in this wording. But we have somebody that exactly pointed us in the right direction. I'm going to repeat the lab. Sodium is low. Bulirubin is very high. Cholesterol is extremely high. With the main fraction being LDL. And the serum osmolality is normal. And that's all you need. You don't need any additional test. Because if you remember that famous or infamous hyponatremia branching diagram. That it comes from every single board exam that I have taken. And the bulk of the hyponatremia is in the middle of the algorithm. Like it's hypotonic. But don't forget about that isotonic hyponatremia. Where the serum osmolality is normal. And as you can see here on the diagram. They give you two causes. Hyperproteinemia. Multiple myeloma being let's say a classical example. Or hyperlipidemia. Which is the case here. Our cholesterol is very high. But here we are dealing with pseudo hyponatremia. Actually the sodium concentration is normal. It's just an artifact of how we measure sodium. And in this case it's lipoprotein exaccumulation. Which is seen with biliary obstruction. And that is why we are measuring low sodium. But actually the sodium is normal. Because if you think of it. You have the serum and you have the solid component. If the solid component increases. That gives you less serum. And the calculation is because we don't directly measure. We recalculate the sodium according to how much solid component is. And normally it's around 7%. If the solid component is much higher. You will lower your calculated serum sodium. There is a direct way to measure the sodium. But it's not used because it's more expensive. That's the direct ion selective electrode proteinopathy. So we did the ERCP. And this is my first initial shot. You see that the wire went most likely in the pancreatic duct. And this is the second shot after injection. And let me see. How do I use the pointer? So here is the obstruction. Which is at the level of the gallbladder. And we passed the wire there. And, of course, above the structure you have dilated ducts. We place a plastic stand. You can appreciate the stand right here. And the question is what is the problem? I'm giving you here an image that I already showed. Okay. So when I ask the next question, everybody can answer except you. Because, obviously, you can come here and actually teach us. Because you're doing excellent. Thank you very much, by the way. So this is anomalous pancreatic junction. And what that is, is that normally the bile duct and the pancreatic duct join together in the intraduodenal portion of the papilla. And here, as you can see, you can see the duodenal contour here. You can see the whitish looking, which is air, in the duodenum, the ERCP scope. And the junction between the pancreatic duct and the bile duct occurs way outside of the duodenum. And this is typical of anomalous pancreatobiliary junction. And just to remind you again, this diagram, orifice, common segment, which then branches into the pancreatic duct and bile duct. And this common segment ends within the duodenal wall. In anomalous pancreatobiliary junction, the junction occurs outside of the duodenal wall. And there is basically two types. Pancreatic duct into bile duct junction, or bile duct into the pancreatic duct junction. And away to the left, you have the normal anatomy. So here is a question that I got on the boards. And it is, anomalous pancreatobiliary junction is associated with type I choledohyl cyst. And you'll get an image of a big bile duct. And if you get that image on the boards, look specifically for anomalous pancreatobiliary junction. Because it is frequently associated with type I choledohyl cyst. But sometimes occurs without type I choledohyl cyst. And if that is the case, it's associated with gallbladder cancer, as in our case. So our patient had anomalous pancreatobiliary junction and gallbladder cancer as a result of that. And if you have that, prophylactic cholecystectomy is indicated, if you do the ERCP, typically for acute recurrent pancreatitis. Because that's the other clinical presentation. So I have lifted this from the internet. It's not my case. But here you have the type I choledohyl cyst. Basically, the bile duct looks like a carrot dilated. And then you have typically relatively normal interhepatics. And there is the anomalous junction here. So this is type I choledohyl cyst. And very quickly, to remind you, the types of type I is what I just showed you. Type II is basically a little diverticulum. Type III is choledohyl seal, which is a cyst within the papilla, basically. And the typical therapy for that is sphincterotomy. And then you have type IV, which is a combination of various interim extrahepatic dilation. And type V also goes by the name of Corollis disease. And freshen up your knowledge on this before your boards, because you'll get at least one question on one of those choledohyl cysts. So if you have type I choledohyl cyst, there is increased risk of bile duct cancer. So that's different than gallbladder cancer. So anomalous pancreatobiliary junction with type I choledohyl cyst. Don't answer, please. What is the typical recommendation that you give to that patient? Exactly. You resect the bile duct. And that's the answer. Anomalous pancreatobiliary junction without type I choledohyl cyst. I already told you. You do a cholecystectomy. Okay. So those are my take-home points. Association of APBJ is frequently associated with type I choledohyl cyst. There is a risk of cholangiocarcinoma. And surgical resection of the extrahepatic biliary tree is the therapy. Not associated with type I choledohyl cyst. Risk of gallbladder cancer. You do cholecystectomy. And again, back to the hyponatremia. Obstructive jaundice can present with pseudohyponatremia. And the key is the normal serum osmolality. There is no need for specific therapy. It's just a measurement artifact. Thank you. Yeah, any thoughts or comments? Not just questions, but of course, questions are more than welcome. How often do you see the pseudohyponatremia? It's uncommon. I've seen three or four cases over a period of 25 years that I have been doing this. Mo, how many you have seen? Very rare. It is rare. Chris? Pseudohyponatremia due to obstructive. Yeah. I mean, it's a similar mechanism to PBC, where they get this high cholesterol, but not to this level. And as you're aware, the LDL is calculated. And that's why the LDL in our case appeared to be sky high, but it's not. It's lipoprotein X. It's uncommon. It's a zebra for sure. My main point was to go over pancreatobiliary junction abnormality, which is also uncommon, but essential to detect. And I threw the hyponatremia because it came with the same case, just as a sidekick. But it's uncommon. That's the short of it. I cannot give you specific numbers, but quite uncommon. What's the cannulation in the anomalous case? No, it's not. Because you have a single common channel, and you have that typical bulbous distribution. So what you see here, it's quite common appearance. This little kind of bulbous and what appears to be stricture about it. I mean, basically, in pretty much all of the anomalous junctions that I've seen, this is present. But because of that, typically cannulation is easy. What is not so easy is recognizing that that's what you're dealing, and you can easily miss it, including on MRCP. The radiologists are not attuned. And I know I don't want to spoil it, but one of the important things that you need to learn is you have to be basically better than your radiologists in interpreting ERCP images and even other imaging, particularly focused on the pancreatobiliary. And I have spent a lot of time, and frequently I'll go and I'll point something to them, and they'll say, oh, yeah, that's there. So obviously, it's not to give me a big head, because I usually know a detailed clinical history. Radiologists just sit there, and they hardly are giving but one little slur of what we put in the request. And the second thing is I may be pretty good at looking at pancreatobiliary, but sometimes there is a huge bone metastasis in the spine that I have overlooked, because I'm not a radiologist. I mean, I can look in my narrow area of interest. Nevertheless, you should be looking at your images yourself and be well-versed. So what do you do if the patient presents with acute recurrent pancreatitis, which is one of the clinical presentations of this? Usually, you do a biliary sphincterotomy, and then you wait, and hopefully decompressing the distal outflow, because presumably what happens is you get reflux of pancreatic juice into the biliary tree, and that's what causes the cancer. So if you decompress downstream, that should be able to help. If this patient develops some stricture, I did not put a metal stent, as you probably noticed, although in unrespectable gold-leather cancer otherwise would be appropriate. But the concern is that the fully covered metal stent will seal off the pancreatic orifice, and you can cause even higher incidence of posterior CP pancreatitis. Obviously, the condition is uncommon enough, so all those are kind of theoretical considerations rather than something that has been proven. But recognize this bulbous appearance of the bile duct. One thing that I defer from many advanced endoscopies, I do inject. I inject gingerly, but I don't like just passing wires basically blindly and relying. So you don't want to over-inject for sure, but a touch of injection can do you a ton of good to make sure you're in the right duct and the wire is not wandering into a side branch and you're thinking you're in the bile duct. Or sometimes the other way around, the trajectory of the PD, you think that you're in CBD and you keep pushing the wire, but actually it's PD and obviously you don't want to do that. A touch of contrast, it's a good thing. And my advice is, particularly for the initial injection, do that yourself rather than the assistant doing it for you because of two things. If let's say you're giving a submucosal injection, you can immediately stop. By the time you say stop to the assistant, another second has gone and they have injected another ml of contrast in the submucosa. So that's my little comments on this difficulty of cannulation and use of contrast injection versus wire injection. To me, all these studies about posterior CP pancreatitis are significantly flawed because they are not blended. There is 20 things that can contribute to posterior CP pancreatitis and it's very difficult to control for all of them at the same time. So I take it with a grain of salt. The main thing I believe is to be gentle. If you're gentle and you don't cause trauma, probably you'll be okay. It's not that much. You can do a catheter guide that I grew during the era of sphincter of audiomanometry. So all of our cannulations were catheter-based cannulations and that's not why we were getting high posterior CP pancreatitis rate. It was the type of patient that we were doing the procedure on. Anyway, I'm talking too much. Any other things before we... For patients with anomalous pancreatic ovary rejunction, let's say they have colic or colic virus, does the speed drop any different? No, I mean, obviously, yeah, good question. You cannot cut to here. You just cut the intraduodenal portion of the papilla. I've not seen a combination of stones and anomalous pancreatic ovary rejunction, but I will just cut the intraduodenal portion and you may want to add a balloon dilation to that, but that's all you can cut, otherwise you'll perforate. Normally, if you cut the intraduodenal portion, you have two orifices in the duodenum, a bile duct and pancreatic duct. This will not be the case. You keep cutting, you cut into the retroperitoneal space, and that's obviously not a good thing. Thank you very much, guys.

ERCP

pseudohyponatremia

gallbladder cancer

anomalous pancreatobiliary junction

personalized treatment

radiological interpretation