Chad Ball 00:12
Welcome to the Cold Steel surgical podcast with your hosts Ameer Farooq and Chad Ball. We’ve had the absolute privilege of chatting with some amazing Canadian as well as international guests over the past year. While the topics have been broad in range, whether clinical, social or political. Our aims for the podcast continue to remain the same. We hope to inspire discussion, creativity, scholarly research, and career development in all Canadian surgeons. We hope you enjoy our second season as we continue to highlight some incredible guests, deliver detailed masterclass sessions on a myriad of clinical topics and introduce some fresh new features such as debate and companion formats. We hope you relish the podcast as much as we do.
Ameer Farooq 00:55
On this episode, we were joined by Dr. Nick Zyromski. Dr. Zyromski is a liver and pancreas surgeon at Indiana University. Dr. Zyromski gave us a masterclass on pancreatitis, covering everything from classification to endoscopic management to percutaneous drainage. We have a very special treat for our listeners at the end of this episode. So stay with us.
Chad Ball 01:36
Can you tell us where you grew up? What that was like and then maybe walk into your training pathway along the way in medicine and surgery?
Nick Zyromski 01:45
I’d be happy to, Chad and Ameer. It’s a real privilege to be here. And I don’t think I’d be going out too far on a limb to say most of your listeners probably don’t know me, but in any event, it’s nice to contribute to this excellent forum. So you know I am currently a Professor of Surgery at the Indiana University School of Medicine. I’ve been here for the last 16 years. This is really… I grew up in Cleveland, Ohio. And nobody in my family was in medicine. But I really enjoyed biology and I enjoyed people and it seemed like medicine would be a good career fit. And it certainly has been. I trained… I went to medical school at the Medical College of Ohio, which has subsequently changed the name to the University of Toledo Medical School that was in Toledo, Ohio. And also did my general surgery residency at the same institution. After two years of general surgery residency, I got connected with a guy named Mike Sarr, who is a GI surgeon at the Mayo Clinic. Mike worked at the Mayo Clinic for his career in Rochester, Minnesota. And I moved to Rochester, Minnesota and did two years of basic science research under Mike’s tutelage. And I will tell you, he was and continues to be one of the finest mentors anybody could ever hope for and a great friend. And so, you know, hugely influential on my pathway in academic surgery. And somewhere along the line, you know, I got turned on to pancreatic surgery. And I think we may talk about this a little bit later. But I realized that I would need to get a little bit of extra training to call myself a legitimate pancreatic surgeon. And so right at that time, Keith Lillemoe and Henry Pitt had come to Indiana and established the HPB surgery fellowship. This was one of the first ones that was accredited by the Fellowship Council. And so I was the first HPB Fellow at IU in 2005. And then subsequently, after Dr. Lillemoe offered me a job and impossible to say no to that offer working with this group and here I am. And now suddenly, you know, a decade and a half down the road, you know, here we are. And of course, we’ve had a series of tremendous fellows much better than me, following me, including Dr. Chad Ball.
Ameer Farooq 04:12
We’ve interviewed a lot of HPB surgeons and they all seem to have this shared love of kind of the complexity of the surgery and the pancreas. What drew you specifically to becoming a pancreatic surgeon?
Nick Zyromski 04:25
Well, the technical complexity of the operations for sure is a draw to all of us. I also really enjoyed the heterogeneous nature of these disease processes, both benign inflammatory pancreatic disease and malignant pancreatic disease. And the fact that there’s a huge amount of thought and decision making that goes into both treatment planning and a lot of times the interoperative decision making with these operations. This is pancreatic surgery, but also obviously, you know, hepatobiliary surgery as well. And I think that really, one of the most attractive things is that there’s a lot of room to go. If you think about the diseases of the pancreas, we have… one of my first mentors is a guy…I mean, I think also the thing that is critical is having mentors and guides. And a man named John Howard was very… I met in Toledo when I was a medical student, John was probably in his early 70s at that point. And John is one of the fathers of pancreatic surgery in the world. He was an army surgeon in the Korean conflict and in charge of the Army Research Unit, and I would really encourage anybody who’s listening here to take a look into John Howard. He was so humble. But such a giant in surgery. He had contributed significantly to the development of the trauma systems in the United States and across the world. And he tackled pancreatic surgery. And it was really some of John’s work in the 1960s, at a time when people were calling for a moratorium on pancreatic surgery that the mortality of a Whipple was near 25%. And John presented a paper in the late 60s, 1968, to the American Surgical with 42 patients, I believe, with zero mortality. And that really emboldened pancreatic surgeons to continue along the track. So, you know, my interactions with John obviously were critical. But he pointed out to me… his words were… we were barely at first base in terms of understanding the pancreatic diseases and unfortunately, you know, now nearly 20 years later, we’re still at first base. So for 300,000 Americans every year who get pancreatitis, there’s no therapy beyond support. So I think the chance to really move the field, to really investigate these diseases, and understand them better and identify points for intervention is a very attractive part of pancreatic surgery to everybody. So anyway, sorry for the long winded answer. But you know, you’re talking about something I love.
Chad Ball 07:27
No, that’s perfect Nick, and your description is dead on of course. You know, John Howard, there’s no question is a giant in many things, including pancreas. But, you know, you’ve become really an international thought leader in terms of pancreatitis, and I think our audience is getting a little flavor of that upfront. So we wanted to maybe leverage that and get you to talk about pancreatitis and walk, really what would be a large general surgery community, primarily trainees and faculty, through some of the current issues that you’ve done so much work on. I was wondering if you could start with just a general sense of prognosticating acute pancreatitis. Obviously Ranson’s is the classic example. But how do these scoring systems, whether Ranson’s Glasgow and so on, with seven or eight of them. Are they clinically useful? How do you use them? How good are we at predicting who’s going to get really sick and who’s not?
Nick Zyromski 08:25
Yeah, I mean, you’re leading off with one of the real open areas in pancreatitis and I’ll preface these thoughts by disclosing the fact that I practice at a University Medical Center, that’s a quaternary Medical Center. So we have a huge necrotizing pancreatitis population. We don’t have an ER at our hospital anymore. You know, so I don’t see people in the ER who are coming in with abdominal pain. I see people who have been outside for two weeks and they’re not getting better. Those are the main pancreatitis patients that we take care ofpredominantly. So having said that, though, once you identify somebody with pancreatitis, I honestly think that clinical judgment is probably as good as Apache, Ranson, Glasgow, the Marshal Score, the Sofa Index, you know, that you need to be a doctor, you need to be a clinician and pay attention to the patient and be aware of the baseline. An 80 year old person with marginal kidneys and underlying coronary disease and diabetes is not going to take a joke. And so when you see an 80 year old person with pancreatitis, regardless of etiology, you know, that patient needs to be in a very monitored, a situation that’s closely monitored, you know? Put that guy in the ICU, put a Foley catheter in and make sure that they’re making urine. Also, be aware, at the other end of the spectrum you know, when you see a 20-year old person, they could have a pretty severe disease brewing, and they can hide it. It’s like the trauma patient who’s good, you know, until they fall off the cliff. They reach that point in the Starling curve and they, you know, or the point in the bleeding where they just can’t keep up. So, there are some very useful. markers. For example, urinary trypsinogen activating peptide has been shown in strong research, some of the interleukins (interleukin two and interleukin eight), particularly the pro inflammatory cytokines are very good predictors. But unfortunately, those tests are really not available widely in clinical use. So, each one of those scoring indices has its own limitation. For example, the Apache score, I was just thinking about working on an editorial. You know, the Apache is great, but it’s really cumbersome if you try to put that into practice and clinical practice, the Ransons, what they call the grave signs, and by the way, we are two degrees of separation from John H. C. Ranson, the very thoughtful surgeon who worked in New York City. Ranson’s criteria came from a retrospective chart review of 100 patients with severe pancreatitis, and they are still very accurate. But the obvious problem with Ranson’s grave science is that you need 48 hours to predict who’s gonna get sick so I guess what I would say is have a very healthy respect for the disease, especially in the first 48 hours. People who get sick with pancreatitis who get really sick, typically declare themselves early. So if you have a healthy respect, have a low threshold for close monitoring, make sure that patients end organs are perfusing. These people you know, it’s been described as a burn in the retroperitoneum that totally soaks up volume, you know, so the mistake that’s made consistently is under playing this and not giving people enough volume, and then you come in the next morning and the guy’s in acute renal failure, because, you know, people are afraid to put them into pulmonary edema. So I think the summary is that clinical intuition in my mind is really probably as good in this day and age as any of these scoring indices. But this is an outstanding area of research.
Ameer Farooq 12:30
That’s the next thing I think is important to kind of review for our listeners, just given the heterogeneity still, with which people kind of talk about pancreatitis, whether it’s surgeons are gastroenterologists, or radiologists. It would be to go over the Atlanta criteria. Can you briefly go over the Atlanta criteria and why that was so important for standardizing the way that we talk about pancreatitis?
Nick Zyromski 12:59
I think the most important…so the Atlanta criteria for people who don’t work routinely in in pancreatitis is based on a consensus conference. And the first consensus conference convened in Atlanta. It was published in in 1992, actually, in the Archives of Surgery by a guy named Ed Bradley. And the goal of that meeting was to try to come up with some consistent definitions. The Atlanta group evolved and met again, and it took like five or six years to do this, it was all done remotely. The current one was published back in Gut in 2013. And Peter Banks, who’s a gastroenterologist in Boston is the first author on that group. And there are a number of gastroenterologist and surgeons and Mike Sarr was a big promoter of that second, the revision of the Atlanta classification. And again, the goal is to get everybody singing from the same page in terms of what are we talking about, perhaps the most important thing. And so out of the revised Atlanta criteria, there came three classes: mild acute pancreatitis, moderately severe acute pancreatitis, and severe acute pancreatitis. And that’s really based on organ failure and the persistence of organ failure. So, the moderately severe pancreatitis has people with organ failure, that resolve and severe acute pancreatitis has persistent organ failure. That’s the fundamental you know, basic definition. And then there are other very important definitions including the recognition of an earlier and later phase of the disease. And perhaps most importantly, is defining what are all these intra-abdominal fluid collections, and necrosis that happens in patients with severe acute pancreatitis. So, as a baseline, about 80% of people with acute pancreatitis, again regardless of etiology, will have relatively mild self limited course of the disease and then about 10 to 15% will have severe acute pancreatitis with variable necrosis of the pancreatic parenchyma and the peripancreatic soft tissue. And those are the patients, the severe acute pancreatitis, necrotizing pancreatitis patients are the ones that we as surgeons are interested in, you know, as HPB surgeons. Because we’re called on to treat these patients and again, I think we’re going to talk in a little more detail about how this treatment has evolved. But the definitions are defining the early peripancreatic fluid collections. And then over the course of the next few weeks, as the body consolidates these collections, and the tissue that’s dead defines itself, then that becomes what’s called walled off necrosis, or WON. And then the necrosis again, like I mentioned, can involve either the pancreas, or the peripancreatic soft tissue, or both. In many cases, it’s both. So again, the Atlanta classification has been an important document that helps us define consistently, what are these phases of pancreatitis? And what are some of the collections? I would be remiss not to mention the tremendous work of John Windsor, who’s a New Zealander, and a brilliant guy, and John and his group have proposed something called the determinant classification, that I would encourage everybody to look up as well. Perhaps not as widely used as the Atlanta but really important because it looks, you know, sort of at functionality in what’s happening through the course of the disease.
Chad Ball 17:19
That’s such an eloquent description, Nick, and I’m glad you brought, you know, the latter classification up as well. I don’t know what your experience over the years is, but certainly within Canada, and my experience was in the US, oftentimes, everyone uses the term pseudocyst. Like everything’s a pseudocyst, in a radiologic report. And maybe that’s because they don’t have the context of time. You know, it’s not a pseudocyst at a week, per se. But I sort of think of that, the lexicon of the Atlanta symposium, very much like the language of grades of, you know, injuries and in poly trauma or staging in terms of cancer. And both of those two things have had really good uptake. But for some reason there still seems to be significant heterogeneity in terms of clinicians understanding and using that relatively common lexicon in our world. Why do you think that is?
Nick Zyromski 18:16
I think we just have to keep pounding that message, you know? I agree with you 100%. This is the single most misused term in pancreatitis, is pseudocysts. And we see it here, thankfully not so much at our place. But in a lot of places, even major places that the radiologist will call any collection a pseudocyst, that’s a critical distinction – what is inside that collection. Because if you stick a drain, or you you know, from whatever, angle percutaneous or endoscopic into a big chunk of solid dead walled off necrosis, you’ve contaminated the necrosis. I mean, the concept of how much necrosis as one of these collections contain has tremendous implications in terms of therapy. So that was one of the main goals of the revised Atlanta classification to make sure people are using this terminology appropriately. And again, still, you know, I mean, we’re still trying to get the message out with a lot of these things. So the other point to add is that these collections are dynamic over time. You brought up the point of time. And even in one person over a week, in two weeks, in three weeks, in a month, in three months, the collections will evolve, even solid necrosis. A lot of times the necrosis will liquefy and turn into a collection that has a lot more fluid in it than it did maybe in the beginning. The final point about pseudocyst is anytime you think about a collection around the pancreas, pseudocysts included, the clinician must consider the pancreatic ductal anatomy. I think if there’s one take-home point from this whole podcast is if you’re seeing somebody with pancreatitis, and there’s a collection, you’ve got to know what’s going on with the pancreatic duct. Because that really, really has a major impact on treatment.
Chad Ball 20:23
Oh, that’s so well said. So, you know, maybe to explore that just a little bit farther and unpack it. You know, as Ameer would say, essentially, the integrity of the main pancreatic duct will drive you left or drive you right. Meaning that if it is intact, the prognosis and the treatment of that patient will be fundamentally different than if its side branch leaks or something smaller. Would you say that’s accurate?
Nick Zyromski 20:45
Absolutely. Yeah. We see in all kinds of patients, major disruptions in the pancreatic… so if the pancreatic parenchyma is involved with necrosis, that’s a much, much more challenging disease process to manage than somebody who has even necrosis of the pancreas, even infected the necrosis. But it’s all extra pancreatic.
Chad Ball 21:09
Yeah, precisely. You know, I would argue too that, and I think you would agree probably that, you know, the left disconnected pancreatic remnant are probably our most challenging cases full stop.
Nick Zyromski 21:21
That’s a very common, very, very common problem that we see. We actually looked at our whole experience with disconnected pancreatic duct syndrome. Tom Maatman, again, one of our outstanding surgery, residents, and researchers have just published this paper in the Journal of Surgical Research this year, and looked at 647 necrosis patients, and 46% of them had the disconnected pancreatic duct syndrome. So that’s, you know, again, our experience is biased for sure, because of our referral pattern as a tertiary referral or quaternary referral place. But yeah, those are really tough problems.
Chad Ball 22:05
I love that paper, that was so well done. I was hoping we can shift gears a little bit here and still stick with pancreatitis for our listeners, but maybe short snappers or not so short snappers, in terms of some some broad headings. I was hoping you could talk about antimicrobial therapy in particular, whether that’s, you know, empiric, prophylactic, or, of course, therapeutic. How do you define that? And how do you look at that? I will reference of course, Tom Howard’s editorial from many years ago, in the Annals, which I still think stands the test of time.
Nick Zyromski 22:38
“As Good As It Gets”, is the title. He was commenting on Pat Dellinger’s multicenter trial, where they tried prospectively to give people empiric antibiotics or not, and found like every other trial, that empiric antibiotics did not decrease the mortality or morbidity of the disease. So the practice pattern should be as a short snapper, as you say, don’t give people empiric antibiotics. Treat defined infections for a defined period of time. If you’re in a situation where you’re concerned about infected necrosis, then I think it’s okay to give somebody empiric antibiotics, not prophylactic antibiotics. But with the caveat that you are treating that patient, you’re treating them for presumed infected necrosis. But you still have to search, that doesn’t stop the search for the infection.
Chad Ball 23:36
This might be getting a little bit nuanced. But sticking with the concept of infection, there’s been a number of papers that have come out, I’d say five that I am aware of anyway, over the past three to four years that look at essentially the outcome in patients with infected versus non-infected necrosis, both in the intensive care unit and outside of it. And it seems through all that literature, I think it’s supported anecdotally, from what high volume centers like yours and ours see: the presence of infection, although as a category infected necrosis may do worse than uninfected necrosis. But in the individualized patients, lots of them are, quote, unquote, “have infected pancreatic necrosis” and their clinical trajectory is really quite easy. And then the opposite of that can be true as well, presumably from an inflammatory driver, as opposed to an infectious driver, and the genic response to that. So I was wondering if you could comment on the realities of infected necrosis because, you know, certainly as a trainee, back when it was all about, do we stick a needle in and define, you know, define what’s infected and then operate on it. It seemed to be very messy, and I think it comes back now at least in our practice, to look at the patient and make the call based on that. So what’s your sense about infected versus non infected necrosis?
Nick Zyromski 24:55
I think it’s really… this is a great topic and definitely, this is is in the weeds for sure. But I love it down in here in the weeds. You know, I mean, the problem with any of these papers, ours included, that try to define infected necrosis is that those numbers are wildly inaccurate. You know, there are people without gas and then necrosis who have infection. I mean, if you look back at Carlos Fernandez del-Castillo did a tremendous paper in the Annals, man, I think probably 2007 or 2010, or something. I mean, one of the main points was that when those guys operated in the (CULTURED) necrosis, when they operated for steryl necrosis, nearly a third of the patients, if I remember correctly, a substantial number of the patients had unexpected infection. The Dutch group has shown that too, and we’ve shown that too. And then on the other hand, when you culture people who you know are infected, and then you go to the OR and clean them out, but they’ve been on antibiotics for 72 hours, a lot of times you don’t get an accurate culture, and so they don’t grow anything. You know, so you say that person is not infected, because you weren’t able to culture it? Even though you know, that clinically, and maybe they have gas in necrosis. You know, so I think that number one is those numbers are really inaccurate. Number two is, I agree, wholeheartedly that we need to be clinicians and treat the patient. However, if a patient has infected necrosis, that is a catabolic focus in their body, and they are not going to get better. Unless that gets treated. There are some people who get better completely simply with antibiotic therapy, with infected necrosis. The vast majority of the patients, however, need some sort of intervention to evacuate the necrosis. And, again, it is a trap to fall into, to just think somebody looks good and put them on antibiotics and send them home for a month. And then if they’re not getting through there, or when you select the resistant organisms or fungus in the retroperitoneum, then their physiology deteriorates to the point. And unfortunately, sometimes we see to the point where they’re not salvageable anymore. So infected necrosis is a big problem, in my opinion. And yes, I agree with youChad completely, that there’s that there’s a huge variance. And a lot of it depends on the host, you know? That’s the thing, you know, I mean, stop me when you need to, because I could talk about this all day, but we are looking at more accurate objective metrics. Elliot Yee is a medical student here. He’s at Colorado now doing his residency. He did a tremendous job. We’re looking for a dynamic frailty index, you know, something that replaces that expert clinician’s gut feeling. What are we looking for, look at the P and I, you know, look at the nutritional index with the, you know, something that can be applied dynamically through the course of this, three months, four months, six months disease to say. Okay, this guy is not getting better, it’s time to step it up to the next size drain, to a new drain, time to take him to the OR before we reach that inflection point in the physiology where they’re not going to tolerate a major intervention. Does that make sense?
Ameer Farooq 28:16
Totally, I think that makes a lot of sense. Speaking of nutrition, I think this is a topic that perhaps is getting more traction, particularly among newer trainees. But you know, there’s been a lot of dogma historically about nutrition in pancreatitis. For our listeners, can you just talk about what the evidence is around early nutrition? And how do you sort of approach that for pancreatitis patients?
Nick Zyromski 28:47
So I’ll tell you, you know, again, I was involved with Karen Horvath, my dear friend from Washington, the University of Washington and a GI group led by a young guy from Hopkins. We were tasked with prospectively trying to look at, systematically all the evidence on nutrition and in necrotizing pancreatitis. It’s all over the board. So the take home messages and again, trying to do this a little more quickly. Nutrition is critical. Early enteral feeding is okay for some. Feed the gut when you can. It’s not tolerated by many. And so in our experience, most people require at least in the early phase, which to me is the first few months of necrotizing pancreatitis. Most people require some combination of enteral and supplemental parenteral nutrition to achieve adequate caloric and protein balance, again in this really massively catabolic state. The other point is that the stomach just doesn’t work in a lot of people. The small bowel works in a lot of people, but especially in people with a big retro gastric collection. You know, that’s the main inflammatory response and there’s a gastric ileus. So, I’m a huge fan of the gastrojejunostomy feeding tube, where you can vent the G part, you can get all the tubes out of the guy’s nose, you can vent the G you can feed the J, and at least you can feed some nutrition into the gut. We published a paper about you know, PEG J and nasal J general feeding tube, Alex Roach is another great residents. Alex will be our HPB fellow next year, did that work, and found that both of them are well tolerated, but feed the gut when you can, but it doesn’t always tolerate nutrition. Now, the third, the next level of thought here is that a lot of patients have mesenteric venous thrombosis in this disease. This is an underrecognized, and another wildly unknown swamp, you know, in terms of what to do, but what I’ll tell you is that patients with SMB thrombus, don’t tolerate enteral nutrition and we have a very low threshold to make sure that they get adequate TPN support: Total Parenteral Nutrition. Again, thinking about what’s the consequence to the liver, especially if that paddock blood flow is compromised. And are there anything you know, special TPN things like carnitine, or things that you can do to potentially minimize steatosis from the TPM.
Chad Ball 31:33
So glad you brought that up Nick. You know, you’ve done some tremendous work, your group there, on thrombosis, and in general, the coagulation system in pancreatitis patients. The pleasure as you know, of reviewing one of your upcoming manuscripts in Journal of American College that we’ll link to in this podcast, but, you know, can you go over the concern about our under prophylaxis of these patients and why that is and how we should maybe measure it and be more vigilant about it?
Nick Zyromski 32:01
Sure, thanks for the pitch. There’s a sweet editorial that accompanies that paper, by the way in the JAGS, so you should link to your editorial too Chad. Again, this is clinical work that’s based on a clinical observation that necrotizing pancreatitis patients have a very high incidence of Venous thrombotic problems. And this includes both mesenteric venous thrombosis that I was just talking about, and extremity venous thrombosis. And so we looked at this retrospectively and found that the incidence was 56%. That’s a huge incidence. Alex Roche and Tom Maatman published a paper not too long ago. And then we instituted a prospective screening protocol for extremity ultrasound screening on a weekly basis for necrotizing pancreatitis patients in the active course of the disease. This is really facilitated by our pancreatitis nurse coordinator, Kathy McGreevy, and you know, that’s another line of discussion. But Kathy, I mean, and I’m mentioning all these people’s names, because these are the guys who are doing all the hard work. You know, it’s a real team effort. In any event, what we found was that yes, indeed, we validated the finding that they have this extremely high extremity DVT rate. And what we found is that by instituting anticoagulation, we prevented symptomatic pulmonary embolism and anybody who didn’t have a contraindication for anticoagulation. Now, that was all background getting to your question, Chad, which is the next layer of investigation is trying to figure out: what is the mechanism of this hypercoagulability of pancreatitis. And when we looked, we have some preliminary data looking at Factor 10A, and found that we are under prophylaxing people with chemical prophylaxis and so, the next step in this work is looking at developing an algorithm to give people appropriate prophylaxis. There are a few caveats. I mean, well, number one, I also must acknowledge that I’ve stolen a lot of these ideas directly from the trauma literature. So to you and all your trauma pals, you know, thank you and, you know, sorry for stealing your stuff but it applies also to these diseases. The one thing that we should discuss, that a potential at least theoretical concern in pancreatitis is the problem of bleeding when we give people very high doses of anticoagulation and that’s, we haven’t thankfully experienced major problems with bleeding up to this point. But that definitely needs to be on the table. And especially in the circumstance where somebody may have a visceral arterial pseudoaneurysm too.
Ameer Farooq 35:15
This is such a neat line of investigation. Shifting gears a little bit. I’m curious what your thoughts are – and this is a real, I think, practical issue that again, sees a lot of controversy and a lot of heterogeneity across different institutions. But where do you see the role of early ERCP in pancreatitis? Is that something we should be doing? Is that, you know, are there certain situations where that’s helpful? Like, for example, if the bilirubin is also concomitantly high? How do you sort of approach that in your mind?
Nick Zyromski 35:51
So the question is in patients with biliary etiology, which ones will benefit from early ERCP? And the answer I think, is really is reasonably as clear as any in this field. There have been several prospective studies, primarily led by the GI groups. And so if somebody is not getting better clinically, in 36, 48, 72 hours… in the first 72 hours, somebody who’s failing to improve clinically, with biliary pancreatitis, and some of the liver chemistry numbers, bilirubin, alkaline phosphatase, are climbing or not falling. Those are the patients who should get early ERCP. Early ERCP should not be done routinely, that’s been shown pretty clearly. The caveat is that this is a tough call, because you can have edema of the intrapancreatic common duct, especially with head necrosis and/or you know, developing head involvement. And so it’s really helpful to have a dialogue with an expert endoscopist involved with this process. When ERCP is undertaken, it’s really important that the endoscopist doesn’t inject the pancreatic duct, because they don’t want to exacerbate the inflammatory response in the pancreas. And we don’t want to introduce bacteria into what is presumably a sterile (in the early days) situation. So you know, the rub with doing ERCP is that you open a gateway to the gut, and that’s an easy access for the gut flora.
Chad Ball 37:36
That’s well summarized. Nick, I want to transition a little bit now to the concept of drains, percutaneous drains in particular. I know you know our senior partner, Francis Sutherland well, and I think every time a drain goes into one of our patients here, a little piece of him dies. You know, and I’ll also maybe just frame it with the caveat that centers like yours and ours, we’re very lucky because the interventional GI groups and the interventional radiologists and us, we’re all so close. And we all treat these patients together in such an important multidisciplinary, multifaceted way. I don’t know how you treat these patients in 2020, to best effect without these complex and heterogeneous groups. But, you know, having said that, percutaneous drains do get put into these patients, usually from elsewhere. Tell us what your overall view of putting drains in collections is, with regard to maybe timing and selection and utility.
Nick Zyromski 38:36
Well, I think you hit another real take home message Chad, which is, treating necrotizing pancreatitis is a team sport. It’s really critical to have a captain of the ship and it doesn’t matter who it is. I take ownership for a lot of these patients but it could be a gastroenterologist, could be an internist, could be a pulmonologist. Somebody’s got to see these patients through this six month course of disease. But there has to be input from the experienced gastroenterologist, experienced interventional radiologists for optimal treatment in this day and age. I feel Professor Sutherland’s pain you know, I mean 20 years ago when I started doing this stuff, we saw somebody with the drain and that was heresy. Into a pancreatic collection percutaneous drain. I think percutaneous drainage is one of the most significant advances that we’ve seen over the past decade and we learned this from the Panter study from the Dutch prospective study looking at the step-up approach. This was validated in Karen Horvath’s study, the percutaneous drainage was introduced back in 1998, by Pat Freeny, who’s a radiologist at the University of Washington. And I would highly recommend anybody interested in this work to read Pat Freeny’s paper from 98 in the American Journal of Radiology. That’s seminal work. He identified the fact that people with disconnected duct don’t do that, well, you know. What we’ve learned about drainage and how we use it in this day and age, you know, percutaneous drainage is often the first step in the step-up approach. Percutaneous drainage really, though, depends on the anatomy of the necrosis. And again, getting back to how do you treat these patients? It’s such a heterogeneous disease, that patient selection and the patient individual situation, you know, how are they doing clinically? Is the necrosis infected? Etc. What’s their nutrition? And really important is the anatomy of the necrosis. Localized collection in the lesser sac, even with a disconnected tail is pretty straightforward to treat. On the other hand, the patient with necrosis is extending down both paracolic gutters, including the lesser sack, you know, multi-field necrosis in a duct disruption or SMB thrombus. Head involvement, I mean, that’s a much different story. But in any event, if somebody has infected the crosis, especially if they have multiple field necrosis, we’ll start with a percutaneous drain. And then, within the next few days, we reimage the patient to see what’s happening to the collection, look at the patient’s clinical progress. If we’re making progress, then we’ll ride it out for a little while. If we’re not making progress, if there’s still a big volume of necrosis, we’ll either upsize the drain or put another drain in, to you know, irrigate one vigorously and have a point of view grass. We’ll consider an endoscopic approach. The Virginia Mason group in Seattle has championed the dual modality, so called dual modality percutaneous endoscopic. But what we found is that consistently, at least a third of the patients will resolve their necrosis with percutaneous drainage. And that’s, you know, again, that’s a huge advance in treating this disease process. I would also like to refer anybody who’s listening to the work of Rajesh Gupta in his group at the PGI in Chandigarh, India. Rajesh does tremendous work in pancreatitis, and those guys have published great work in the Annals and other surgical journals about use of TPA streptokinase. And most recently, hydrogen peroxide, he’s injecting the drain to try to break up and liquefy the solid necrosis. And again, John Windsor’s group has done seminal work in this area to. John’s looking at trying to isolate the compounds in leech saliva, you know, which one of those…I’m sorry, maggot saliva, not leech saliva. And you know, the maggots eat dead tissue, but they don’t eat live tissue. And so, which one of those compounds might be available, you know, we haven’t sent them any in a while, but for a while, we were sending necrosis over to New Zealand so that those guys could take a look at which one of those compounds liquefied in necrosis.
Chad Ball 43:10
I think you’ve touched on so many important points there. And you know, I mean, maybe I would take the liberty of summarizing it, which is, you know, at the end of the day, the multidisciplinary nature, again, is so critical. Because I think when people read, you know, you and I write a paper on transgastric necrosectomy. The perception from the outside is often like, they operate on everything, or you read a nice percutaneous paper, they put drains in everything. And really, that’s not the case. When we sit on panels, we usually all agree on exactly what to do from all these different disciplines, more often than not. And so, you know, I think you’re right, the group has to be a collective, and it has to be a single unit working together, you know, with lots of different heterogeneity and backgrounds. That’s the only way we’re going to get these patients better.
Nick Zyromski 43:58
Super terrific summary. I think we’re inching there incrementally. I really think that, I mean, it’s a heterogeneous disease, there are multiple approaches, oftentimes, multiple approaches are useful for the same patient over time. And I think that, a lot of times, I’m invited, you know, like you say, I’m known for this disease and I get called to talk at GI meetings and a lot of times I’m the sacrificial surgeon on a panel of gastroenterologists. And my message is, look, this is a team sport. I mean, we got to get away from the mentality that my way is better than your way, you know? GI is superior to surgery, surgery is superior to GI. Percutaneous trumps everything. You know, that’ just not true. Every modality is important for one patient or another. And the trick is figuring out which patient needs what approach and when.
Chad Ball 44:51
Exactly and the other thing that you touched on that’s so very important is the longitudinal care of these patients. You know, banging in a drain and walking away is not going to be helpful. Putting an endoscopic stent in is not going to be helpful. If you do it once and you’re not willing to take those patients back over and over and debride them through, you know, a big axiom stent or something and the same thing applies to us. It’s just that historically, I think in most places, surgery does provide that longer term care as opposed to some of the other other types of services. But certainly in pancreatitis centers, that’s clearly not the case.
Nick Zyromski 45:26
You know, the median time to recovery from necrotizing pancreatitis is almost six months, for patients who don’t die early. You know, this is a long term problem. And what we’re finding out is some of the even longer terms, which are fascinating, you know, duty and duodenal strictures, bile duct strictures, endocrine and exocrine insufficiency, you know, rare but crazy things. l mean, we’re looking right now actively with a GI psychologist at what Marty Freeman termed “post pancreatitis stress disorder”. You know, every single one of these patients is depressed. When the surgeons are making this diagnosis, I’ll tell you, it ain’t subtle, you know what I mean? But what can we do up front to intervene, you know? We borrowed some of your guy’s work about mindfulness interventions, you know, we’re going to apply some of that work. I’m a musician, and I’m fascinated by the effect of music therapy. We’re going to try to do some music therapy to try to address some of these important, holistic and long term problems with this.
Chad Ball 46:35
Well, I mean, that’s so beautifully said. And, you dance on an indirect topic there, which is really how we communicate this to patients on an individual level. I mean, I learned from you guys, but usually up front, I say to these folks with really bad necrotizing pancreatitis that, you know, this is probably going to take a year out of your life. You’re gonna look back at 2018 and say, “wow, that was a crazy year”. And if it’s shorter than that, I think they’re happier. And the worst thing you can probably do is undersell it upfront, especially if you’re not comfortable with the diagnosis in the long term management to these folks.
Nick Zyromski 47:08
Yeah, I think that’s a fair take home point for everything, always paint the picture darker than it may be, you know? Then when they get better, they say, oh, man, Dr. Ball, he must be a great surgeon, I got better in six months instead of a year. Honesty. Honesty, that’s they key.
Ameer Farooq 47:28
Speaking of operations, your group and the Calgary group collaborated on a great paper talking about trasgastric nectrosectomies. And it was interesting, you know, when we were studying for our equivalent to the American board exams, the Royal College exams, talking to other residents across the country. And I’d say probably the majority of institutions really didn’t have a lot of people doing necrosectomies this way. I’m certainly biased because I’ve had the opportunity to watch Dr. Ball and some of the other HPB surgeons in Calgary do this and I think it’s a great operation. Can you describe what this operation is? And sort of why your groups really felt that this was a good way of dealing with pancreatic necrosis?
Nick Zyromski 48:21
Yeah, thanks for the shout out. I think that Michael Driedger was the was the one of your contemporaries, probably, or junior residents who was really important in a lot of the important work here. Obviously, Dr. Ball shepherded this paper through. This was a multicenter study with Calgary IU and Brendan Visser and his team down at Stanford. And so, the question is, how do you approach somebody with a transgastric pancreatic debridement? First of all, determining which patient is appropriate for transgastric pancreatic debridement is important. And so, we highlight the fact in the manuscript that this is a really select group of patients with necrotizing pancreatitis, probably 15% at most of everybody with necrosis. And the ideal situation is somebody with necrosis that’s confined to the lesser sac that with or without disconnected tail. If somebody has biliary pancreatitis, surgical transgastric debridement – and transgastric debridement can be approached endoscopically too of course. There are trade offs, but if somebody has biliary disease, you can take the gallbladder out and do a cholangiogram at the same time. The way we approach it, we’ve done a few of these laparoscopically and we find that it’s easy enough to do with a short, upper midline incision. We use ultrasound religiously, and ultrasound helps define, I mean, it’s usually not hard to figure out where the location of the necrosis is, but you can see how much fluid and how much solid necrosis is there. You can see what the vascular flow is and the relationship of the necrosis to the vascular structures. You can interrogate the distal bile duct with ultrasound. Once you get good enough, that’s another advantage. I think it’s important to think about the presence of the left side of Portal hypertension. So the splenic vein often is thrombosed. And the short gastrics and the epiploics have huge varices. And so you can get into some bleeding getting through the stomach, but we make an anterior gastronomie, use the ultrasound to localize where we’re going to make our posterior gastronomy. You can potentially get disoriented and get into the retroperitoneum, not into the necrosis. So that’s, I would say, be careful trying to get through the back of the stomach. Oftentimes, it bleeds and if it bleeds, you got to open it up a little more counter intuitively, you got to open it up so you can see what’s bleeding. It’s easy enough surgically to stop this venous bleeding with compression and suturing. I like to put a big GI stapler to make a cystogastrostomy to make that hole as big as possible. I use a seam guard, and then I oversew that whole thing with a prolene suture, again, because of the potential venous bleeding in the wall of the stomach. Debriding the necrosis is an art. And the trick is just take what comes out easily. Because you don’t want to debride the interior wall, the portal vein. If there’s a major hemorrhage, you can pack that area. You need to pack it, especially if it’s a big cavity, you got to pack it with a lot of laps and then do your kocher maneuver so you can get your hand behind the SMV and the portal vein and give a little posterior pressure to see what you’re into. But once you get the necrosis, debride it, irrigate it thoroughly. And then basically close and enter the stomach in whatever way you want. I think the stomach a lot of times is really thick. And so I like to sew everything rather than stapling the gut. Do your cystectomy, image the bile duct. Please, please, please image the bile duct in some way, shape or form. And biliary pancreatitis, you don’t want to leave a small stone. And then, you know again, depending on the clinical situation, you can put a feeding tube in, you can put a GJ tube in to decompress that stomach if they haven’t been able to eat. If it’s somebody who’s like walking wounded, you know, they’ve been home and eating but they’re just, you know, have early satiety and pain and flu like symptoms. I don’t always put a GJ tube in, but I definitely am not shy about that either. And so I’d say it’s easy enough to get access to the gut, it’s easy enough to pull that tube out when people don’t need it. So that’s sort of a summary. Indications are important. Operative approach. Do the gallbladder. We’ve actually published a few videos. Tom Maatman is the first author on a couple of videos that are out there, one in Journal of GI Surgery. I can’t remember where the other one is, but there’s some interoperative tricks in those videos.
Chad Ball 53:13
Oh, that’s a perfect, eloquent technical description. You know, maybe just to summarize two other points and one to leverage on yours, which is that patient selection for this is critical. We can’t be operating on the wrong patients. Otherwise, things certainly go sideways with this technique as well. The other thing, of course, is just really gentle, soft, cautious tissue handling, no matter whether it’s from the very start to the incision, or all the way into the last stitch. The educated finger and inexperienced fingers certainly helpful but really soft. And just hoping to close out here, to ask you about two other things. The first is that you have a tremendously close and large family, your wife I hope it’s okay if I say is also a surgeon. You guys have an amazing group of kids. You are a family guy, how do you balance all of that? How do you balance life and work and music? And before you say it, you know, you can’t start with “not well” because I know that’s not true.
Nick Zyromski 54:18
You know, I think balance in life is something that is so critically important. And everybody through my life, I’ll just speak to my own experience, but I have been wildly imbalanced at various points in my life. And I married up for sure. Jennifer Zyromski, MD surgeon, wonderful doctor, even better mother, very tolerant wife, and you know, she keeps me in line man. I mean, she tells me what I need to do and when I’m not doing enough, you know for the family. So I think having a partner in a relationship is really important. Jen and I, a few years ago, we decided we’re going to take one day off during the week. You know, we have six kids, the ages of our kids are 14 through five. We didn’t plan to have that many, they just kept coming. And you’d think two doctors might have figured that equation out. But in any event, and that’s the most beautiful thing in the whole world, for both of us, you know, but it’s also the hardest thing. Tom Howard told me this Chad, when we were having our first baby. He said, congratulations, it’s the best thing you’ll do. And it’s the hardest thing to do. And you know that as an awesome dad, yourself, I know you are. But you know, it’s a huge sacrifice. And it’s a sacrifice, when you love what you do at work. And you get the rewards for doing that at work, you got to be able to put that aside. And it’s been really helpful for me to have a checkpoint, you know, check in with my wife. COVID has been really interesting. We’ve shut down the travel, you and I were talking before we get started, we basically shut down the travel. We’ve been home a lot, our OR log dropped for a while, you know, and it was great. And I will tell you, as conscientious as I think that I am about trying to put my family first, man, I was way busier than I thought I was. This kind of stuff creeps up. And so just trying to be aware of where you are, you know, periodically sitting down to evaluate where you are, personally with family and professionally. Jen and I – I started to tell you – a number of years ago, we decided we we were going to take a day off during the week, in the month. And again, when I was training, this would have been heretical to say that we were going to do this, but the kids were in school. At that time, we had some young kids, but we had a nanny helping during the day. And we just take the day and hang out. You know, a lot of times we don’t do anything crazy. Maybe we go to Costco or we go to see the financial guy periodically, or we definitely have lunch. We have a good lunch and it’s a great way to just say okay, you know, let’s slow down and reconnect and figure out where are we and what do we need to address. And at night time, it’s crazy. And everybody’s tired on the weekends when the kids you know, there’s 11 different sporting events and somebody’s play, and something. I mean, it’s just, you know, it gets to be 10 o’clock at night and you’re exhausted. And so finding time in the day to talk about things and to be together when we’re fresh, I think has been a very important thing that we’ve done to help keep balance in our life.
Ameer Farooq 57:59
I’m gonna immediately take that tip and hopefully when I’m a staff guy, try to incorporate that into my life. It’s such a great piece of advice and great tip. I did want to dig a little further into your passion as a musician as well too. And Dr. Ball has actually played for the residents your pancreas blues song as part of his pancreatitis talk. And it’s fantastic. And I understand that you actually recorded that with another pancreas surgeon, Claudio Vacci, from Italy as well. Can you talk about how you sustain that interest as a musician and how that’s been an outlet for you?
Nick Zyromski 58:46
How much time do we got? I mean, this segues from the balance piece, you know. I think another really important part of balance is to find something to do outside the hospital. We love what we do. You know, we’re surgeons, we love doing surgery, we love taking care of patients. And, you know, fundamentally, there’s no more rewarding job on the whole planet than helping another human being. But, you know, it also takes a huge psychological and emotional toll. And I think that finding a way, you know, to express yourself creatively outside of the hospital, you know, through some art work or whatever you do. I mean, everybody, you know, a lot of people are athletic, and they run and I do that, too. And I think that’s great. But having a creative outlet for me has been a really fun and important part of my life for a long, long time. And I’ll tell you, you know that also it’s fun to walk in those circles because musicians are cool guys, and they have a totally different view on the world than surgeons do. I’ll tell you that. Claudio Vacci is a hero of pancreatic surgery. He defined…he got the ISGPS together (International Study Group of Pancreatic Surgery) and wrote that seminal paper about speaking of definitions, the definition of a pancreatic fistula. And so, Claudio is a tremendous musician, really beautiful player, a really beautiful writer. And he has a lot of recorded stuff that’s out there that you can listen to. So, Bill Traverso was in charge of the Pancreas Club. The Pancreas Club was honoring Claudio Vacci for his lifetime contribution to pancreatology. And Bill called me up, if you have any knowledge of Bill Traverso, he is one tenacious guy. And he said, look, you know, Claudio is a musician, you’re a musician, you should play something at the dinner. And I said, no, Bill, I don’t want to do that. And he said, no, you really have to do that. And I said, no, I’m not interested in doing that. And then he called me back. He said, hey, you got to play some music. And I said, no. And he said, well, at least call Claudio, you know, and I said, fine, whatever. And so I emailed Claudio, and Claudio said “of course! We play some music!” And I said, all right, well, whatever. So we’ll play some music at the dinner. The dinner was in Washington, DC. And then I thought, well, maybe I’ll write a song, “the pancreas fistula blues”. And play it for Claudio. And there it sat like that. And then it got to be like a week before the meeting, and I hadn’t done anything. And so I called up Jeff Matthews. Jeff Matthews is the Chair of Surgery at University of Chicago, great pancreatic surgeon, great musician, also a really articulate songwriter. And I said, Jeff help! And he was like, haha, good luck buddy, and he only hung up. So I wrote this tune on the way out to DC on the plane. And Claudio and I played it at the dinner. And it was beautiful. I mean, because we had a captive audience of like the 200 people in the world who would actually appreciate this tune. We’re all in the room. And so it was pretty fun. And then I thought, well, I’ll bring it back and record it with the band. And a couple years later, the Pancreas club was in Chicago. And so Claudio called me up and said, “hey, I’m coming to Indy, to record the lead guitar”. You know, so we brought Claudio back. And so Claudia’s playing the lead guitar on that track. And we just had a beautiful time. And I think that, you know, I mean, again, there’s so many layers to this, how beautiful is it for the International relationship and the music and things like that. But it’s, you know, for me, music is a great release. And it’s a great connection with people. And it’s a great creative outlet. You know?
Ameer Farooq 1:02:45
The last thing we’ll ask you, Dr. Zyromski, is if you could go back in time and give yourself advice as a trainee. What would that advice be?
Nick Zyromski 1:02:57
I’ll tell the audience that Ameer and Chad were kind enough to send some of these questions ahead of time. So this is not completely off the cuff. And I’m really glad that you did send these questions because this is an important point. And I think that the things we were talking about: balance in life is probably one of the most important things that I missed when I was a trainee. We love what we do as surgeons. Surgical training is a major league upfront sacrifice to achieve your expertise. And there’s no substitute for experience. But, you know, the way that we did it back in the day when it was every other night on call, and, I mean, essentially giving up a decade of your life in the hospital of good years, you know. It was very sad to see contemporaries getting their, you know, lake house and boats and stuff like that, starting their families and, you know, we’re in slugging it out in the trenches. And there’s no way around that the experience piece but you know, somehow trying to dial in a little more balance upfront and paying attention to your physical health. Paying attention to what you eat, paying attention to, outside of the hospital, hobbies and looking for mentors to help you find this balance. You know, I have been unbelievably fortunate in my life to have so many beautiful mentors. Mike Sarr, Keith Lomo, Henry Pitt, Tom Howard, Attilah Nakeeb. And the list really just goes on. Jeff Matthews, you know, who was kind to me for no good reason, beyond the fact that he’s a great guy and he’s interested in an academic surgery. But those people, you know, they don’t just fall into your life a lot of times. It’s okay to go looking for a mentor, look for somebody who you admire, look for somebody who you want to emulate. Look for somebody who’s got something that you want, you know? Chad ball has all these incredible diverse interests. How do I be like that? You know? And you don’t need to have a mentor that you meet with on a weekly basis, I happen to work in a lab where I got really close to Mike Sarr, you know, but you can take a lot of different mentors and take little pieces from all of them. So I think you asked for one piece of advice, but it’s sort of two pieces of advice, which is balance and mentorship. And I don’t have a perfect equation to achieve either one of those things, but both of those things take work. It may sound funny, but it takes work to achieve balance. It takes work to develop a relationship with a mentor. And so those are the those are the ideas. (Audio begins: “Pancreas Blues” by Nick Zyromski plays.)
Ameer Farooq 1:07:27
You’ve been listening to Cold Steel, the official podcast of the Canadian Journal of Surgery. We’d love to hear your feedback and comments. Send us an email at firstname.lastname@example.org or tweet at us @CanJSurg. You can check out all of Dr. Zyromski’s music on his Spotify channel, and we’ve put the links in the show notes. Happy 2021. (Song continues).