E134 Masterclass with Charles Vollmer on Cystic Neoplasms of the Pancreas (Part 2)
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Chad Ball 00:12
Welcome to the Cold Steel podcast hosted by Ameer Farooq and myself, Chad Ball. We consider it an absolute privilege to bring you guests from around the world who are truly experts in their craft. Our mission is to offer you a combination of not only masterclasses on clinical surgery topics, but also insights into achieving personal growth, productivity and fulfillment as both a surgeon and, perhaps more importantly, as a human.
Ameer Farooq 00:42
Dr. Charles Vollmer is the chief of GI surgery at the University of Pennsylvania and is a passionate pancreatic surgeon. This is the second part of our masterclass series with Dr. Vollmer on cystic lesions in the pancreas. In this Part 2, Dr. Vollmer dives deep specifically on IPMNs, giving us an in-depth discussion of types of IPMNs, the various guidelines for IPMN management, as well as an overview of operative principles for resecting IPMNs.
Chad Ball 01:10
Just to take a moment, then, and summarize, before we move on to a particular specific topic, when we think about these cysts — so we have serious cystic lesions, serious cystic neoplasms, which are generally benign. We have pseudocysts, of course, that are, by definition, benign on the oncologic spectrum, certainly — not on the inflammatory spectrum. We have mucinous cystic neoplasms, or mucinous disease, that is certainly more concerning. And then, within that spectrum, we have the IPMN. And I think we — probably all 3 of us would agree [that] we see radiology reports every day that say IPMN all over the place, which we know is probably not the right terminology; that's really a pathologic diagnosis [that is] more difficult to radiologically diagnose, but could you frame for our listeners and our learners, the different types of IPMNs, whether it's main-duct or side-branch or mixed-duct, and how you approach that whole topic on its own.
Charles Vollmer 02:11
Okay, so just before that, what you started with there is this categorization, so we didn't go into some of the radiographic features, but those different things you have greater features. They also go with the demographics of the patient, and they go with the history and physical as well. So we can largely call a Cirrus cyst adenoma for the most part, by its radiographics. And that's benign and that basically, in many cases, you can just stop looking at it, okay? There's some nuance to that, but that's, kind of, where it is. The mucinous cystic neoplasm is a singular lesion. It happens once in your pancreas, okay? So, unilocular lesions are there that way. And then the pseudocyst stuff will largely be in line with other parenchymal changes, and history of pancreatitis, drinking, these sorts of things, but also parenchymal changes in the duct system, calcifications, these kinds of things, so you get a lot of other clues to get that out. Now, we're going to, sort of, by eliminating those, you get down to this thing, that's the default, which [is] IPMN. So, intraductal papillary mucinous neoplasia; all of those words have meaning to them. And, in essence, its epicentre is the ductal epithelium in any place along that duct. Papillary, meaning there's going to be a [inaudible] or a growth element to it, or a heaping element of abnormal tissue. The M for mucinous is very important, indicating that this is a metaplasia or dysplastic change to mucinous excreting cells in the pancreas that puts the [inaudible] cells turn into mucinous excreting cells in the pancreas. And then that, basically, is this process. And the neoplasm is the general term for growth — abnormal growth. It used to be called tumour; the World Health Organization had a lot of semantics over this. It's not that all these things are actually invasive cancers and such, so neoplasm was the more generic proper term for it. So IPMN tells you all about that. Now, let's get back to the duct part of it. It's essentially — I tell the patients, as I show them a picture of pancreas, that you have this main duct that is macroscopic; it's 2 mm to 3 mm in size normally, but it is macroscopic. You caught it. You can see it, actually. Think of that as being like the Nile River, the Amazon, the Rio, okay? These are — it's the main courseway, and it's going to go out to the bow at the Delta, the [inaudible]. That's going to be fed by all sorts of side-tributaries that are actually microscopic. You have to look under the microscope to see these things in real life. So, those are called side-branches in our terminology, and then ultimately, at the back end of that is a cul de sac. And you know, from your — remember, your pathology elements were basically all the [inaudible] cells are situated around the cul de sac of [inaudible], right? So just get that image of a tree in your mind, inside a ductal tree inside of the pancreas. If it is derived in the main pancreatic duct, it is more aggressive, more virulent, so to speak. And we would quote a chance that that could become cancer at about a 50+ percent rate. Red alert. Alarms going off. [You've] got to be on top of that, kind of thing. If, on the other hand, this is derived in the side-branch elements or the periphery of that tree, the cul de sac, so to speak, that side-branch variant is far less aggressive, and can be about a 5% or less chance of developing a cancer in it. So there's this discrepancy, for sure, on where that is. And then there's this third category, which is a little bit of both. It's called mixed-variant, with both of them being radiographically or, ultimately, pathologically involved. That tends to act like the main duct. So any main duct dilation element to this is going to be — or involvement, ultimately, on the path — is going to be on that aggressive side of things. I kind of make a couple of other analogies for the patients to help understand this process. First of all, you can think of this as being like a cherry hanging off of a vine. The main duct is the vine, the stem is the side branch, and the cherry is the cyst. And that's how it looks radiographically. And you're always sort of trying to say it; "Well, can you see that communication that sort of confirms that?" Alright? And the second analogy I make is: this is a process kind of similar to a babbling brook in the woods. So, it's sort of, just, trickling along, and then the beaver comes along and piles his sticks up on it and blocks it. And what happens there, well, it backs up. The pond is behind it, okay? So that's what, you know, conceptually, these side-branch cysts are within the parenchyma. Now, what is that blockage? It could be 1 of 2 things. I don't think any of us know this directly, but the blockage is in this microscopic side-branch element, and it could either be the viscosity of the mucus that's being excreted, is just a plug within the very fine channel, and it's an obstructive process that way. Or it could, in fact, even be the disease process, sort of, heaping at the cellular level, impinging in on a microscopic calibre to cause the blockage of it, and then the cyst itself actually is just sort of a physical bleb behind it or maybe involved with it. So that's, sort of, my conceptual process on this. The other thing about this is multicentricity. Serious cyst adenomas are singular. Mucinous cystadenomas are singular lesions. So if you have a person that's got a singular lesion, then you have to start to think "Could these things be involved?", but really, the multiplicity of IPMN is it's a calling card for that disease process. And the reason we would think about this is that biologically, we believe that this is probably a field defect process, genetically or at the machinery-level of the cells in the pancreas.
Ameer Farooq 09:37
There's all these criteria that trainees are taught and we had to study about for our exams, the Sendai criteria, the Fukuoka criteria. How do you think about those criteria when you're looking at an IPMN, and can you go through those criteria for our trainees?
Charles Vollmer 09:55
Alright, so obviously, everyone and their brother, academically, you know, is intrigued by this and wants to get on to it, and there's just a plethora of the guidelines, and a lot of these are driven by societies and different interest groups in the field. So you've got radiographic interests, you've got gastroenterology interests, you've got surgical interests, etc. You talked about [Fukuoka]; that's really, sort of, like the Bible on this. It was the International Association of pancreatology got a bunch of wise people together in the early-2000 zone to describe this process clinically, and then put guidelines for management of the mucinous lesions, essentially. And so they came out with, sort of a — it was a review of the literature at the time to get them to the point. And then there are a number of new [inaudible] radiographically. How do you surveil over time, and then when would you need to get aggressive because of the threat of a cancer? So those are really the bedrock, okay? And the other things have sort of been built around them. And I'll skip through any detail of those — I'll basically say how I talked to a patient about it, and how I think about it. So essentially, you're looking for a number of triggers, that are going to say there's a higher likelihood of this being cancer. Of all the players that we see with IPMN, only 10% of them in today's world will now go to an operative endeavour, and fewer than 5% will have cancer — you know, biologically, of all the people, fewer than 5% will have cancer. So when you go to the operating room, you're still not having a complete fidelity between, "I'm going to take a cancer out" and "I took a cancer out." So about half the time, you're actually taking low-grade dysplasia out still, despite this. So we're looking at certain indicators that would say you're going to be at the higher range of chance that you're going to have a cancer in situ or higher when we take it out. So, those features are: size of the cyst. The general original number was 3 cm. That was based on some very old literature that they used for that guideline development. That was the 80s and 90s, and just early surgical resection stuff that basically said, a 3-cm cyst has about a 20% chance or more of having cancer when you take it out, because that was based on surgical resection, gold-standard kind of stuff, not, "3 cm left in the body; I don't know if it has cancer or not," okay? The general idea is — the quote was that if you had a 1-cm cyst, you had an under 1% chance of having cancer. A 2-cm cyst is 2 to 5 cm, and a 2%–5% chance, and a 3-cm [cyst] was 20[%]; therefore, there was an inflection point, and boom. There it goes. You better worry. Well, you can look at the flip side of that and say, "Let's use a little common sense." There's an 80% chance you don't have cancer in that 3-cm cyst. So for about a decade, there, in the early 2000s, a 3-cm cyst was an absolute: you go to the operating room. You got to take it. And we've learned after the fact that so many of those cases we've taken, we've taken out and they are on the early biological end of that disease process. Maybe it was unnecessary. You can argue about that, okay? So now we're actually tempering the enthusiasm about large cysts. What I do now with that, instead, unfortunately, we do believe the larger there is, the more surface area of disease; you could be more vulnerable. We still look at them, and we kind of tighten the leash on the surveillance of them to a tighter timeframe. And the 3-cm cyst is actually where I would go to the biopsy. And I would want to go say, "Okay. The size alone is one thing. It's got some sort of risk, but why not go to the heart of the matter? Suck the fluid out and see what we can know more directly." Alright. So size is one criteria. You should also realize that as you age, the size of cysts will go up. As you age, the chance of you having a cyst is more prevalent. So, about 15% in the population will harbour a pancreatic cyst overall, but if you're 70, it's more like a 40% chance. And as you age, your system will get bigger, so it's acquired and it moves on biologically that way. Let's move to the next thing. Next thing is a mural nodule. A mural nodule is a hump or a heap. Obviously, it's very intuitive to us; that's a growth that's probably neoplastic at the very least, and maybe cancer, okay? So, the presence of a mural nodule found, usually best on endoscopic ultrasound, but sometimes MRIs, but you have to have a big map. Like, you don't get mural nodules in 1-cm cysts. You can't really discern that kind of thing easily — 2 cm, even at that. It's usually got to be something that's got a big, you know, ying-yang to be seen, right? The mass is the negative image in the cyst, kind of thing. So, mural nodules are there, and they can also be confounding, in that you can get mucus — dense mucus plugs — within these that look like solid mass elements or thicker elements to things that mimic a growth. And that's better seen by the ultrasound, where they can — and also by contrast imaging — to determine if this thing takes up contrast or not. So mural nodules, if you really believe it, that's a bad thing. And I would say that when you see that it's, in my mind, a more sure thing you're having cancer in that specimen, maybe closer to, like, a 75% rate when you operate on that and take it out. So that's a bad kind of thing, but you're limited to — you have to be a bigger [inaudible] farther along the road to really see that. The next thing would be, obviously, overt cytology. You put the needle in, you get the cytology out, and it says it's got high-grade dysplasia or higher, well, bingo. There you go. You've got to move. You've got your proof, basically. Then you get into the dilated main pancreatic duct. So that is vexing here, okay? And it's kind of interesting, because sometimes you're looking at one of these cases, and you're saying, "Is this pancreatitis?" Or — there's no mass in the pancreas, but you've got this dilated duct and like, is it a pancreatitis problem, or is it IPMN, right? So we're basically talking about a side-branch round lesion that then has a duct element that's dilated with — something's going on there, and it's usually at the point where the cyst is. And it's — you can conceive, is there an obstruction process going on, in some way, shape or form, from the disease? And you got to think in your mind conceptually, well, that's something grabbing or choking around the duck, it's probably a cancer — neoplastic cancer process. And yes, a dilated duct is associated with cancer, more likely. It then gets to the shades of, you know, calibration of that duct. So, 2 to 3 mm is your norm, so what if you have a 5-mm? Well, you can see that it's obviously different and bigger, but it's not really terribly bad. Are you worried about that? Do you wait until it's 7 or 8 mm? The general cutoff in the guidelines would say 1-cm–wide duct or larger is the trigger; it's the go time, with that. I would argue, you could say that any form of that duct dilation smells like more advanced disease, because you have more of a chance that you're actually dealing with the disease in the main duct; it makes it main-duct or mixed, and then, therefore, you're in this 50+ percent chance of harbouring the aggressive tumour. So those are that, and then the last thing I would say is that the trigger we have currently is symptoms, which are going away as time has gone on. When I was a surgical resident, we were coming in with people with these gross pancreatitis problems, and you'd look at their imaging, and the cystic disease was just overwhelming the pancreas parenchyma and the gland. So, you know, this has been stuff that had been allowed to sort of fester and get to that point, and then it makes the symptoms. But it doesn't have to be so over over the top. You can get symptoms otherwise, and the things we care about are jaundice, and overt, clear-cut pancreatitis. So both are pretty evident and obvious. Sometimes you have the subtle pancreatitis case of: the person's got it. And they get it — "Oh, it's not a big humdinger." And they get over it pretty well, and they have a recurrence of it over a temporal timeframe. And then someone decides, well, let's take a look in there and they say, "Oh, well, yeah, your pancreas doesn't look good." That's one route to get to us, but generally it's true pancreatitis. And why is this, again? The ducts system is blocked. Either it's the pancreatic duct for that, or you're getting — you're picking off the bile duct with the process, and it causes the jaundice. Overt jaundice is one of the biggest triggers for: there's cancer in there. In fact, either of those symptoms — if you have a symptomatic presentation, the highest correlation of all the things we've talked about, is those 2 things, that there's a cancer involved. And so, you're going to act in an operative manner to treat that. And secondly, you're going to act in an operative manner to help your patient who's symptomatic from it, right? So there's an obvious reason to be operating on those cases. So that's your spectrum of clues. The newer things on the block are a little bit more nebulous and less proven. [Cancer antigen (CA)] 19-9, not from the [inaudible] flu, but from [...] So yeah, that's your indicator: potentially pancreatic cancer. But yes, false positives [inaudible] that by inflammatory changes in the pancreas. So, you know, there's a lot of controversy; should you be getting serum CA 19-9s on everyone at the outset when you meet them? Are you hunting for that cancer by looking at that tumour marker? Well, beware if you use it, because you can get shnookered. I have more than a handful of patients who have elevated CA 19-9s, but proven track records of surveillance without any lesions or cancers developing within it. The other thing would be rate of growth of assist at about 5 mm or more over a year or so — a year to 2 years. That worries people. All these cysts, for the most part, are going to have some sort of advancement in their size. Some stayed pretty stable for a long time, but if you look at them over a decade or longer, they're going to creep up in size, so you've got to expect [that] that's just part of the gig. But the question is, are they basically taking off with a rapid change that has been associated with a higher chance of cancer and get — and now is a more modern trigger for us in terms of the guideline. So that's how I think about it. I'm hunting for those things. And the other thing about it is, now, it used to be early days that we would choose one of those things. If you had one of them involved, you had the justification to go for it; now, it's more like, well, I've taken these things out, and I found that half the time, I don't have — I just have low-grade dysplasia when I take it out. It was not cancer, and it wasn't at that point, etc. So now we're getting a little bit more discerning about this, and particularly, like, a 3-cm cyst alone, if it's clean, does not have a nodule in it, and there's nothing else going on; I feel very comfortable watching that alone. So now you've talked about the concept of accumulating these triggers to be — and I bet that if someone did the study and looked at, you know, the the combination of A, B, C, D and E, all together, there's going to be an escalating proof of cancer being in those kinds of cases. I don't think anyone's actually done that, but that would be, sort of, where we are. But that's how I think about it when I'm trying to make the decision as the surgeon about that very, very rare 10% chance that you need to have the operation.
Ameer Farooq 23:31
Dr. Vollmer, in the patient that doesn't have those high-risk [inaudible], doesn't have particularly worrisome findings on either imaging or [endoscopic ultrasound], how do you follow those patients? Is that with CT or MR or — how do you — and how often do you follow them? Yeah. So, you know, basically, we're at a place here because of the nature of this, this can become cancer, and we can't tell in any given patient who that — where that cancer will develop and when, okay? We are handcuffed. We do not have a biological signature yet. There's no blood test. There is no AI machine-learning aspect on all of our radiographic stuff that's going to say, "I can tell you, Mrs. Jones, that you have this premalignant thing, and in 18 years, it's going to blossom. What would you like to do about it? Do you want to take it out now and forget about it forever?" Kind of. "Or, do you want to wait this out and watch it?" So, we just don't have that personalized medicine place yet for this. And because of this and the nature of the cancer— and we, as the practitioners, are now, sort of, on the hook for this medicolegally, in a way, okay? So if we were to say, "Don't worry about it, [there's] literally only a 5% chance you'll ever get cancer. [inaudible] can go away. Don't worry about it. It'll never happen. The odds are in your favour. It's not going to happen to you, okay?" And we absolve ourselves of the responsibility of looking at that. You're going to get shnookered one day. It's going to happen to them, and they're going to say, "Well, you knew about this and you blew it off. I'm going to sue you." Okay. So here we are; we've got to do something. Right now, I think we're in the adolescence of this disease process, in terms of our intellectual mastery of it. We know a lot, but there's so many questions still in there. We're not in a mature decision-making process–level with it yet, and so we're still dependent on that. So, one of the advantages to this surveillance process over time, generally using MRIs, which are noninvasive and non — they don't give you radiation in the process. By doing this, we're accumulating massive amounts of data that hopefully we can learn from and pattern over time, so there's an advantage of that kind of thing. The patient, themselves, wants this to be done just for their clarity and their sense of mind. You start talking premalignant; you bring that into the conversation, they perk up, okay? You know, and then it's very hard for these people to get this off their mind. When they come to get their surveillance imaging every year, they're worried. And it isn't until you give them the good news [that] everything's status quo, stable, nothing changed in the last year, it looks exactly the same. You tell them that, I mean, they let the breath out in front of you, like, "Cool. Wow. Great. I feel better about that. Thanks." And then they forget about it a year and then they — it strokes up when you do your imaging. So the general idea here is you're going to image them somehow. CAT scans on a yearly basis is really not palatable in terms of the, you know, the radiation risk — it's also not the best test for it. We default to a year because it just seems right. I mean, it's like, it's a good time post, you know, time frame in time that you can just say, "Well, it's a long enough period." Think about this if you're imaging and watching people: the shorter interval you have, of any sort of observation of anything, the less you're going to be able to discern change, okay? When you live with someone on a daily basis, they look to you the same all the time, even though their hair is growing and their skin's changing and all that kind of stuff. They sort of look — you can recognize them being the same person. When you are absent of them for 3 months or a year or something like that, and then you see them for the first time, you're like, "Oh. Wow. You look different. You changed," right? So you have to have that, sort of, temporal absence. And the longer you go with it, the better, for that. So I'm a little leery about these ideas of, hey, let's get a scan every 3 months, which obviously is expensive and that kind of stuff. You've got to, sort of, have that distance between the two. So we have just, basically out of defaults, said, "Well, a year sounds good for a follow-up," right? The other thing I can tell you is personally in our own system here, we cannot put someone out farther than a year in terms of ordering their test through our health care system. We can't, like, give a [prescription] and say, "Come back 5 years from now with the MRI." They won't be able to put you — order your — put you in the system, so, logistically. So a year is where we've, kind of, settled with it. I have actually moved to, for these early, tiny-ditzel, under-centimetre kind of things, I've moved to every other year, because that threat of there being a problem in this short period of time, and particularly when you're talking [about] older people, you know, what's the point in looking at something that's probably not going to turn foul. So I'm doing it on an every other year basis. We figure the logistics out in the clinic and get them ordered up for that. So that's, sort of, where we are with it. But the truth is, we're beholden to it. And therein is the biggest dilemma of our field right now, and that is: resource utilization, about this. So think about this: If I say 15% of the population can be found with an incidental cyst, maybe you do the numbers; millions and millions of people out there. And you're gonna say, well, now this becomes part of your regular health care maintenance process, just like getting your colonoscopies, your mammograms and the likes. Well, now we're beholding you to a CT or an MRI every year. What if you're 40 years old? You're going to do that for 40 years, huh? This is a problem, right? And for those of you in the health policy range, this is an enormous thing to attack, is like, how are we going to find the value of this screening process? Particularly since we're talking about a test that's about, let's say, 1000 to 1500 bucks a shot for its optimal test. That makes a ton of sense. You know, the last question, particularly, you know, keeping in mind the fact that I'm a nonpancreatic surgeon, and many of our listeners will be nonpancreatic surgeons, I'm just curious; when you're in the operating room, what are the principles that you, sort of, follow or have in your mind when you're doing this operation? Particularly, you know, something that comes up on exams is, you know, are you really having to chase a negative margin while you're in the operating room? Are you having to take frozen sections? Do you ever have to do total pancreatectomies for IPMNs? How does that — what are the, sort of, your principles for IPMNs in the operating room?
Charles Vollmer 30:49
That's what makes our field intriguing, and it's also the vexing part of what we have — we have to make these decisions, and they're not easy. So the first part is, it's, that all starts in the clinic. And it's by the size-up of your radiology and progression in time and whatever is going to do — whatever your history and story takes you, but usually about the radiographic imaging. So the idea has been that, in the past, we would favour a targeted pancreatectomy. There's even places in the world, particularly Germany, where they will go — and the Far East, as well — go pluck out a cyst; essentially an enucleation operation. And they'll go back again on a patient 6 years later, and do that kind of thing, etc., etc. It's a very unappealing thing to me to be making crevices and pockmarks into the pancreatic gland and thinking that that's going to go well. But it's always the balance between preservation of parenchyma or not, and taking the disease out. I told you before, we don't know, biologically, if this is true, but we believe it to be a field defect, because so many times we get our pathology back and it describes — first of all, you've got multiple lesions on all over that are grossly there, but sometimes, you take a singular lesion, a macroscopic lesion out, and the path comes back, and they will tell you that there's microscopic changes indicative of IPMN inside branches at the margin, or some other place in your parenchyma, etc. So we've got that proof that this is the case. The question is, in any given patient, is this a universal truth? Or are there some patients where there's just a focal epicentre of disease? And it's possible that [that's] case in some people, alright? So the general idea is, you want to talk about targeted pancreatectomy, because the idea of taking out all the pancreas, which we can do, and I would actually say, IPMN now is the primary qualifier or condition for which we do total pancreatectomy, moreso than cancer or even pancreatitis. So, and that's when you're talking about a gland that is riddled with — the whole gland is full of it, okay? And this is just, sort of, like, you size up the eye of the beholder, the degree of the involvement of the main duct, and the likes. But we just don't know. You have — you couldn't have a head that's got a dominant cystic area, and then you've got this dilated duct behind it; it will look very similar to a pancreas cancer, except instead of a mass, you have the cyst in front of the dilated duct. You don't know what to do. Should you take the whole gland out? Does that whole main duct have a disease? Does it not? Guess what? When you go in and cut those things out, you're going to find all of those answers. You're going to find clean ducts, even though they're dilated, so they accommodated up. You're going to find ducts with low-grade dysplasia. You're going to find main ducts that have the high-grade dysplasia or cancer at them. So it's just sort of a crapshoot where you are, but we would err on the side of minimal operation, or a partial pancreatectomy, first, and building up to that is as necessary. Your singular lesion cyst in the uncinate process, normal duct otherwise, you're going to do a Whipple and you're going to — you're not even going to check the — I don't even check the duct at that point. It's a normal-sized duct, etc. You're going to have a confidence that your disease process was focused where you got it, you took it out, and that's that, okay? Now, doing the frozen sections is tricky, because you're reliant on your pathologist, and this is not easy pathology for them, and there you are with, "I can't tell," or, "Oh. The duct was totally denuded. I can't even give you an opinion," etc., or, "I see dysplasia here, but can't firmly tell you if it's high-grade or not." Alright? So, you got that. And I would tell anyone who's doing the surgery, my principle here is that this begins in the office with the patient. If you have a main duct dilation, and it goes out past that tail or neck region and such, you better prepare the patient for the possibility of getting the total pancreatectomy, and that really is smarter to do at the office visit. And while it's a little bit overwhelming, and daunting, it's a balance here, because you can freak these patients out about that. "Well, I may have to take all your pancreas out," and explain that, right? Well, that can be really upsetting at that point in time. But it was a lot more upsetting as — "I did this operation and you came out of it," and, "Oh. I took all your pancreas out. It was necessary," okay? So you're going to shock in one place or the other, and I think it's always better to have that figured out. And I also, sort of, barter with the patient ahead of time, like, you got to understand, like, the consequence of doing a total pancreatectomy if necessary. If necessary, great, but if I've got an equivocal call here, and I believe it's in your best nature, that there's a good chance you've got bad disease left on the other side, but I can't prove it, I kind of need a license from that patient ahead of time. I'd like that license; that, if that's necessary, you can do that. So I have some pretty deep conversations to stuff up at a time. The bottom line to your question is, we're in, sort of, no man's land with this. The general idea is that you can cut a margin, and if it's high-grade or invasive cancer shown there, then you are obligated, basically, to take the rest out, unless the patient couldn't tolerate that, If you're doing this on an 80-year-old person, you're basically going to say, "Well, I'm not doing a total pancreatectomy on you. Unfortunately, we're going to have to leave this disease behind," you've basically done a glorified major biopsy on the patient. So there's nuances to all of these kinds of things, but high grade or higher, you're going to want to go chase that and take that out. But we definitely have literature that says: low grade, you can sit on, and you don't — you know, you're leaving some behind. And you can surveil that because, remember, you're looking at largely nonradiographic disease at that point, and you'd be looking for these bigger triggers of radiographic criteria and such that would indicate more than it's at the high-grade dysplasia when you get to that point. So the other thing to know about this, though, is, we used to say, "Oh, we'll take that out. We got your cyst out great. We took that premalignancy out." Oh, you're absolved of this; it's over — no. That's not the case. There's actually very real evidence that there can be recurrence of this disease process in the rest of the gland, and that can be in 2 forms: it can be new cysts popping up — in other words, that field defect moving on and happening elsewhere — or it can be a de novo different solid pancreatic cancer, and that risk is on the order of about 3%–5%. The chance of developing another cyst is on the order of upwards of 20-some percent. But guess what? You're obligated pretty much for the rest of your life if you have IPMN, whether you did the operation or not to get surveillance with an MRI after the operation. So these become long-term patients for you. And I welcome them back every year with a surveillance MRI of the remnant pancreas. I have rarely in my career had to act on that yet, okay? In other words, something changed on that and I had to go back, but my career may not be long enough, actually, to get to that point. So you take something out on a 50-year-old, they have some remnant disease, it may take them another 20 years before they get to the point where they have to have the completion pancreatectomy. So, that's sort of where we are with that. It's a fascinating biological thing that we have no mastery of, and we're sort of gamblers in a way, in terms of what we're doing with things. I'd say, to wrap up, you know, the conversation here, we've come a long, long way from the onset of my career. When I started, I'd remember having these talks and fellowship — "It's a cyst. It's premalignant. It's likely IPMN. That's got to come out." It was a knee-jerk reaction. "We're going to go to surgery for that." And we are so, so far along with that now, with so much more sophistication in our thought process, but still plagued by a lot of question marks.
Ameer Farooq 40:21
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