I have the privilege of being able to speak about acute pancreatitis today. I wanted to just give you a little bit of a brief background in my clinical history, just so you kind of know where I'm coming from. When I initially started, I started in solid organ transplant, so liver, kidney, pancreas transplant. Did that for several years before migrating over to GI, and I really have been primarily focused in GI oncology and pancreatic obiliary since I joined, so 13 or 14 years now. This is one of my favorite topics, and I was really happy that they had asked me to speak to everybody today on this. I wanted to go through what's new in 2023. To start, we'll go through just a brief overview of what acute pancreatitis is, and then we'll talk about the evaluation and management. I also want to go into some of the potential causes of acute pancreatitis and management strategies by those cause, and then I'll give you a little bit of just some take-home tips and points. And so what is acute pancreatitis? It's an inflammatory disorder of the pancreas and the peripancreatic tissues. There may be multi-organ involvement. It is the number one GI cause for hospitalization in the United States, with a median hospital length of stay of four days. There's actually increasing incidence of acute pancreatitis, and unfortunately, there has not been appreciable improvement in outcome. And the CAT scan picture that you can see circled in red, there's a lot of peripancreatic edema there. And so what causes acute pancreatitis? Well, the number one cause is still gallstones. Number two, just closely behind that, is alcohol, and this is looking at the United States. Iatrogenic, so after ERCP, medications, trauma, autoimmune, hypertriglyceridemia is something that a lot of people think about, but it's actually pretty uncommon, pancreas divisum, hypercalcemia, hereditary pancreatitis, pancreatic tumors or cystic lesions, and then idiopathic. And so this is a MRCP image that shows a common bile duct stone, again, circled in red, and what you can see above that is that that common bile duct is dilated, and then the intrahepatic ducts are too. And I always explain this to my patients, you know, think of a big maple tree. That main trunk is your common bile duct, as it branches off into those smaller branches and ultimately the leaves, those are your intrahepatic ducts. And so when something's blocking way down low, you're going to see everything else get a little bit larger. And those dark spots that are within that red circle are the stones. And then this is an ERCP image, and so if you can see my cursor, this dark right here is the ERCP scope, and this is their wire coming up through. All of these little white opacities here, those are stones in the common bile duct. And then this is a CT image that shows a dilated common bile duct, again, with all of these little white spots, which are stones sitting in that duct. Medication-induced auto-pancreatitis is, it's rare. So acute pancreatitis can definitely happen because of medications. And a lot of times, again, we think about it, we look for it, but less than 5% of cases are related to medications. There are several which can cause it, and that's why I put this little graphic there for you guys. But most commonly, and the ones to kind of just keep in the back of your mind would be azathioprine, furosemide, hydrochlorothiazide, estrogens, sulfasalazine, and Bactrim. Takeaway from this, medication-induced acute pancreatitis does not happen often. Prognosis is excellent. You should get rid of the medication, and in most cases, you're not even going to attempt to restart it. The only time that you might is if it's really an unclear situation and that medication's strongly, benefit of it is strongly preferred over the risk. And so the one situation I can think of offhand would be somebody who's on a chemotherapy medication that maybe could cause acute pancreatitis, unlikely, and they have other reasons, like alcohol use. In that case, alcohol use is probably the more likely reason. And so you may resume it, but if there are other options, that might be the better choice as well. Pancreas divism is the most common congenital malformation of the pancreas. About 3% of everybody in the world has this. It is the failure of the dorsal and ventral pancreatic ducts to fuse. And so what happens is the majority of drainage, all your pancreatic juice and fluids and digestive enzymes ends up flowing through the minor papilla instead of the major papilla. The majority of patients who have pancreas divism are going to be asymptomatic. Over 95% of patients with this do not have any symptoms. Small subset, 5% or less, may have recurrent acute pancreatitis though. And so in pancreas divism, if we look at that graphic for a second, your major papilla where usually everything is draining from is the one circled in green. In pancreas divism though, all of that dorsal pancreas, instead of being drained from that major papilla goes out the minor papilla. Secondary pancreatitis, again, is not very common, but it is something that we need to be able to recognize. Most commonly, this is a variant of the PRSS1 gene. That's an autosomal dominant condition. There are genes that are autosomal recessive that also can cause it like the SPINK1 and the CFTR. And what's important to remember about these patients is they have a significantly higher lifetime risk of developing pancreatic cancer. So it's up to a 50% lifetime risk of pancreatic cancer. Autoimmune pancreatitis, where your immune system essentially doesn't recognize your pancreatic tissue as your own and starts to cause inflammatory response. Two types, there's type one in which you have IgG4 positive plasma cells. That's the marker for disease. And in those cases, your serum IgG4 will often be two times the upper limit of normal. There's also type two, which is characterized by granulocytic lesions. In these cases, there is no IgG4 positivity and there's no systemic involvement. Autoimmune pancreatitis can have pancreatic and biliary manifestations. And so this could be a mass forming pancreatitis, or you could get a prominent head of the pancreas when you look at imaging, either CT scan, MRI, or even endoscopic ultrasound. They may present with mild to moderate abdominal pain, and they could develop pancreatic duct strictures, biliary manifestations, or obstructive jaundice. And you can also get biliary strictures, either the common bile duct or those intrahepatic ducts. And this is an example, again, this is an ERCP film. So the white here is your scope. And this is a stricture of the bile duct that happened in a patient who had autoimmune pancreatitis. And so for the first polling question, just to make sure everybody's coming back from lunch and still awake, which of the following can cause recurrent acute pancreatitis? Pancreas divisum, hereditary pancreatitis, autoimmune pancreatitis, or choledocholithiasis and microlithiasis. Exactly. So all of these can cause recurrent acute pancreatitis. So what's a presentation of acute pancreatitis? Well, patients will complain of sudden onset epigastric pain. This is often a deep seated, moderate to severe pain that will typically radiate to the back, maybe worse with oral intake. You may find them kind of tripodting or leaning forward because that helps to alleviate some of the discomfort. This pain can last for days when it's really severe, could be weeks or months, and it may be associated with nausea and vomiting. On physical exam, I always start with systemic signs and kind of work my way down. So systemically, patients may present with fever, tachycardia, and hypotension. And on an abdominal exam, they'll frequently have that epigastric tenderness with guarding and rebound tenderness, and they may have decreased or absent bowel sounds. Developing an ileus during acute pancreatitis is not uncommon. The revised Atlanta criteria is often used for our diagnosis. And so this is abdominal pain that's consistent with that acute pancreatitis. So that deep seated sudden onset epigastric pain with an elevated serum amylase or lipase more than three times the upper limit of normal. And the upper limit of normal for these tests varies widely depending on the lab. And so I didn't want to put a definite number there. Definitely pay attention to what your lab reference ranges are. And then a characteristic findings of acute pancreatitis on imaging. So I need two of three of these criterias diagnostic for acute pancreatitis. How do we evaluate? So we have an index of suspicion a patient came in with this typical type of pain. The first thing is usually labs. So liver function tests, fasting triglycerides, IgG4, if you have a suspicion for it, BUN and creatinine, calcium, hemoglobin, hematocrit, and your white blood cell. Why do we do these things? The LFTs, the triglycerides, and the IgG4 are going to help us determine the cause. And then BUN and creatinine, calcium, your hemoglobin, hematocrit, and your white blood cells are predictors of severity. And so looking for elevated liver function tests will make you more suspicious for a biliary pancreatitis. So something like gallstones, choledocholithiasis. Those elevated triglycerides, when you have super high triglycerides, so we're talking usually well over a thousand, is when you can get hypertriglyceridemia-induced acute pancreatitis. IgG4, like we mentioned, for autoimmune pancreatitis. And then for the predictors of severity, we're looking at BUN and creatinine because of intravascular volume depletion, hypercalcemia, again, intravascular volume depletion, and infection. So particularly patients who have those stones or even the autoimmune pancreatitis patients who maybe have some biliary strictures could present with cholangitis. And when we're evaluating a patient, you want to be looking for SIRS criteria, systemic inflammatory response syndrome. So we've done our blood work, what do we do in regards to imaging? There's a few different imaging tests that could be helpful. Ultrasound to look for those common bile duct stones, if you have an index of suspicion for that. Free air series. So patients who present with that acute abdomen, particularly when you're starting your workup before you know that their lipase is super high, a free air series might show a localized ileus. Chest x-ray is a good thing to do really in the terms of looking for severe disease. So there's a high frequency of pleural effusion with severe acute pancreatitis. Abdominal CT scan is actually not usually needed for diagnosis. We only use that for specific indications. And so how do we grade acute pancreatitis? Mild acute pancreatitis is characterized by the absence of organ failure and local or systemic complications. And another way to put that as patients who come in, they don't require ICU stay. They have a length of stay less than three days. Moderately severe acute pancreatitis. They don't have any organ failure or they have transient organ failure, less than 48 hours. So that would be typically a length of stay less than seven days. And then severe acute pancreatitis, there's persistent organ failure, more than 48 hours, and it may involve one or multiple organs. And so that would have a length of stay over seven days and or an ICU stay. Prognostic scoring systems also exist, and there are several of them which I've listed here. There's Modified Ransom's, Apache 2, the Harmless Pancreatitis Score, SERS criteria. In general, a lot of these have limited utility. And the reason for that is that they aren't great for sensitivity or specificity. They do require a lot of lead time to calculate the score and they have limited predictive value. And so for many of these, you either can't calculate it till you're 48 hours in, or you have to calculate it on admission and then repeat it again 48 hours in. And so hard to say when you've already had a patient who's been there for two days, how much is going to change. For severe acute pancreatitis, a few things that we're looking for. So local regional complications, that pancreatic necrosis and sequelae secondary to that. The systemic complications is really important. I think of all of our predictive scores, SERS is probably the most useful. It's the one that we can immediately identify, it's the one we can immediately act on. And these patients can develop that multi-organ system dysfunction. So we see respiratory failure, you can see renal failure in these patients. These are patients who require ICU care. There's a high morbidity and a high mortality. And the treatment really centers around being able to provide excellent supportive care. So that ICU, management of SERS, and then drainage of fluid collections when they occur. And so I just wanted to highlight there are guidelines related to this. This is gastroenterology of 2018, the AGA guideline. And then ACG also has one which had come out a little bit older, this is 2013. So the first thing for acute pancreatitis is often hospital admission. Patients come in, nothing to eat or drink, IV fluid hydration, and it's really goal-directed fluid management, which I'll talk a little bit more about. Vomiting control is important for these patients. They're really uncomfortable. And sometimes, many times actually, a short course of narcotics is not unreasonable for these patients. Also anti-emetics, that nausea and vomiting can really be debilitating for them. You want to monitor their urine output, their hemoglobin and hematocrit, their BUN and creatinine, and their vital signs. So you're watching for intravascular volume depletion and hemodynamic instability. If they're not able to take oral intake within two days, consider enteral nutrition. And then finally, the intervention that's specific to the cause of pancreatitis. And I put this last intentionally, because the first thing we should be doing is addressing the patient's current status. And then secondarily, we look for what's the cause and then how do we address that cause. Nutrition in acute pancreatitis, initially these patients are coming in and you're not feeding them. You really want the pancreas to rest. Only need to place an NG tube if there's an ileus or vomiting. That's really more for the gastric decompression. When you do begin refeeding these patients, we often will start with a higher carbs versus fat or protein. Carbohydrates stimulate the pancreas less. In mild disease, food can be started once the pain and markers of inflammation are improving, which is usually within 48 hours. In severe disease, you want to start refeeding within a week at the longest. And that's because it's a high catabolic process. These patients start to lose weight and muscle mass quickly. And in these cases, a nasal jejunal tube is preferred. You're passing it beyond the ampulla. And so you're not stimulating the pancreas this way. IV fluid recession is super important in these patients. And if you had asked me a few years ago, I would have said IV fluid, IV fluid, IV fluid. But this was a landmark trial that was published last year in the new England journal of medicine called the waterfall trial. It was a randomized controlled trial of 249 patients. These patients received either aggressive IV fluid, which was a bolus of 20 milliliters per kilogram. And then they had their baseline IV fluid infusion of three milliliters per kilogram per hour, or they were in the moderate IV fluid resuscitation where they only got a bolus if they were hypovolemic and their baseline was 1.5 milligrams per kilogram per hour. And what they saw was that the patients who got the aggressive IV fluids actually had a significant increase in adverse events. So they stopped the trial at interim analysis. That's why it was stopped at 249 patients and 20% of patients in that aggressive arm versus 6% of patients in the moderate arm had a increase in fluid overload without a significant impact on your clinical outcome. So they didn't see that by getting the higher IV fluids, we were actually making an impact on reducing the moderate to severe or severe pancreatitis. Prophylactic antibiotics are not recommended in these patients routinely. Now there are some people who need them. Those who present with biliary sepsis or cholangitis, if there's a documented intraabdominal sepsis. And I added this last point because it's important if you're thinking there's an infection, if they start to spike a fever or something like that, you have this high suspicion, you want to get your blood cultures, work them up. In those cases, empiric antibiotics for a short time while you're working that up may be appropriate. What about ERCP and acute pancreatitis? Well, it's indicated for biliary sepsis and cholangitis, documented CBD stones. If there's a pancreatic duct disruption or leak, they can develop a pancreatic fluid collection. And so an ERCP with a stent placed in the pancreatic duct is indicated in those patients. It should not be a routine procedure in all patients. And it does not reduce the severity of pancreatitis or the duration. Surgery traditionally has been used for necrosectomy and debridement of those pancreatic fluid collections. It really has been almost entirely replaced by endoscopic fluid collection management at this point. For patients who have bowel ischemia or other intra-abdominal catastrophes in the severe situations, they may need surgery. And then it is indicated for people who present with gallstones and CBD stones. And so that gallstone pancreatitis, they should have a cholecystectomy. When should we take the gallbladder out? The cholecystectomy within 24 hours of admission, reduce the number of ERCPs, time to surgery, and 30-day length of stay. And that's been shown in a few studies now. Same-admission cholecystectomy has been shown to reduce the 90-day healthcare system cost. And patients with severe acute pancreatitis may not be a candidate for that same-admission cholecystectomy, but you should do it as soon as possible. And so general take-home is if you can do it within 24 hours or at least the same hospital admission, then that would be ideal. There are a lot of complications of acute pancreatitis. So pancreatic pseudocystis is probably the most common. About 25% of patients will develop these. They do develop after a matter of weeks to months. And so when we were talking about imaging and we said CT scan is often not needed for diagnosis, if they have a moderate to severe, severe pancreatitis, a CT scan may be appropriate after a number of weeks to months to look for these fluid collections. Pancreatic necrosis can develop multiple organ failure, like we've talked about. Pancreatic duct structures and obstruction, biliary obstruction, duodenal obstruction can happen because of all the inflammation, particularly if it's the head of the pancreas. Malnutrition, pleural effusion, pancreatic pleural fistulas, and pancreatic ascites. And so this is just a CAT scan image. Those dark gray fluid collections that the arrows are pointing to are the pseudocystis. And particularly of the smaller one, you can see there's a well-defined wall around it. If patients have pancreatic pseudocystis and they're asymptomatic, observation is appropriate. You don't have to intervene on these in asymptomatic patients, but you should follow them. And so contrast enhanced CT scan or MRI every three to six months. If patients are symptomatic, so presenting with abdominal pain, biliary obstruction, sometimes it's actually early satiety and inability to tolerate oral intake, because if it particularly the kind of the head of the pancreas area where the stomach is, if your stomach can't expand because it's pushing up against this fluid collection, then they could get some weight loss. You can do drainage. So frequently it'll be that step-up approach. It'll be endoscopic management. And then if endoscopic management is ineffective, you can step up to percutaneous or hybrid of both, and then ultimately going to surgical if needed. For symptomatic rapidly enlarging or infected pseudocystis, this has been shown to be quite effective. The success rate is up to 95% and the recurrence rate is generally less than 20%. And just a couple images of what it looks like. And so if we start on the left, there's a large pancreatic pseudocyst, nine by 11 by 13 centimeters. Four weeks after going in and doing an endoscopy using an ultrasound, identifying that fluid collection, putting a stent that goes between the stomach and that pseudocyst and draining the pseudocyst that way. Four weeks later, you can see how much it's gone. And then nine weeks, this little white right here is just the tip of that catheter and the fluid collection is significantly smaller. And so some practice pearls, the incidence of acute pancreatitis is increasing. Management remains challenging. Early diagnosis, goal-directed fluid therapy and prevention of multi-organ dysfunction and necrosis are the goals of therapy. The prognostic scoring systems, they exist, they're TDS. SIRS evaluation and management is probably the most useful clinically. CAT scan and antibiotics have specific indications, should not be done on everybody. Ventral nutrition is critical. If they're not able to resume their oral intake, then you should start to think about that naso-dejunal feeding tube. Non-invasive imaging with endoscopic ultrasound and MRCP is recommended when needed. So if you're looking for things like strictures or stones, particularly if you have an abdominal ultrasound that's not diagnostic, an ERCP is indicated for cholangitis, common bile duct stones and PD strictures, but should not be invoked in everybody. Thank you. I'm going to turn it back over to Jill now.

acute pancreatitis

clinical history

prevalence

causes

supportive care

complications