So we're going to start off this afternoon with acute pancreatitis, and I did this in a case-based discussion format, so there's a couple of polling questions as we go along that I'll have you guys answer. I don't have any disclosures. And so my objectives today are really to provide a brief overview of acute pancreatitis, look at the evaluation and management of acute pancreatitis, and then I really want to discuss some of those causes and the appropriate management of each one, and then we'll summarize it at the end. And so my case study, this is a 45-year-old male who presents with acute onset severe epigastric pain. He has a history of GERD and diabetes, a surgical history of laparoscopic fundoplication. He takes sitagliptin and pantoprazole. He does smoke about half a pack of cigarettes a day. He used to drink heavily in his 20s, but hasn't had any for over 10 years, no recreational drug use. Family history notable for a sister who has a history of pancreatitis of unknown etiology, and there's no known family history of pancreatic cancer. And so some blood work was done, showed his white count was 12.4, his bilirubin was normal, his AST, ALT normal, lipase was over 5,000. Had an ultrasound initially, didn't show any CBD stones or any gallstones. Then he had a CAT scan, and CAT scans are not always indicated in acute pancreatitis, but he was in the emergency room and that was done, and so you can see that there's quite a bit of inflammation and fluid around the pancreas, which is consistent with acute pancreatitis. And acute pancreatitis is an inflammatory disorder that involves the pancreas and peripancreatic tissues. In severe cases, it might have multi-organ involvement. It is the number one cause of hospitalization for GI reasons in the United States, and that median hospital stay is four days. It has been increasing in incidence, and I think importantly is that there's really been no appreciable improvement in outcome. There are a lot of different causes of acute pancreatitis. The two most common are gallstones and alcohol, about 45% for gallstones, 35% for alcohol. I think it's important to really know the other causes though, because when we work up somebody, these are the things we're going to be looking for. And so certainly post-ERCP, you would get that from a history or a chart review. Hypertriglyceridemia, autoimmune pancreatitis, pancreas divisum can cause recurrent pancreatitis. Medications, hypercalcemia, hereditary pancreatitis, trauma, and then idiopathic. Medication-induced acute pancreatitis is rare. It's only less than 5% of cases. Lots of medications can cause it though. Some of them are listed in this chart here. Just put it here for reference. I think importantly, knowing that it doesn't happen often, but the prognosis is excellent. And if somebody does have medication-induced acute pancreatitis, we want to make sure that we're discontinuing the offending medication if possible. We presented a case report at American Pancreatic Association in November with a patient who had a vast and induced acute pancreatitis. And interestingly, he was completely asymptomatic, but his lipase was in the thousands. His CT imaging showed that there was acute pancreatitis, and he actually developed a pretty large pseudocyst from it. And so the first polling question, what additional evaluation would be helpful to determine the etiology of pancreatitis? A pancreas biopsy, ERCP, triglycerides, potassium, or urine tux? And this is in related to the case we're talking about. Perfect. Yeah. So pancreas biopsy is not indicated unless there's a pancreatic lesion or a target that you're looking for. You can actually cause pancreatitis if you're biopsying normal pancreatic tissue. ERCP is rarely done for diagnosis, and typically it'd be done therapeutically. So if you do have somebody with recurrent pancreatitis, and we'll talk about a couple instances where you might want to do pancreatic duct endotherapy, that would be an indication, but not really to evaluate the cause of pancreatitis itself. Triglycerides is the correct answer, hypertriglyceridemia, typically over a thousand can cause acute pancreatitis. Potassium level doesn't, calcium would, but not potassium. And then urine tux, you know, theoretically you could find some chemicals maybe, but not something that we would typically do. And so when we look at lab studies that we can do to work up acute pancreatitis, I grouped them into two categories. The first three might help us determine the cause, and then the next four are really predictors of severity. And so if we look at them one by one, your LFTs can be a sign of biliary pancreatitis. So think of those gallstones. If they're coming down the common bile duct, if they're blocking them or obstructing them, you could get an elevation in your liver function tests as well. Triglycerides should be fasting, but high triglycerides can cause acute pancreatitis. And then IgG4 can help you look for autoimmune pancreatitis. For your severity, the BUN and creatinine is going to help you assess for intravascular volume depletion. Same for your hypercalcemia, hemoglobin or hematocrit for your intravascular volume depletion. And then you're thinking about infection with your white blood cell count. This can be a little bit challenging because we know that inflammation can also increase your white blood cell count. And so you're looking for other systemic signs of infection as well. And so we want to make sure we're monitoring for SIRS, that systemic inflammatory response. And I wanted to highlight there are a couple of guidelines. And so as we go through things, I am kind of referring to these guidelines when I give any generalized recommendations, but know they're available, read through them, kind of familiarize yourself with them. And so the management of acute pancreatitis is hospital admission. You want to do pancreas rest, so nothing to eat or drink, aggressive IV fluid hydration. And they refer to this as goal-directed fluid management. And so what that means is that you're giving that five to 10 cc's per kilo per hour, often somewhere around 400 cc's per hour. Usually it's lactated ringers. If they have high calcium, then you'd want to do normal saline instead of LR. And then you're really monitoring for their intravascular volume and repleting it as needed so that hemoglobin and hematocrit should not be going up in these instances. Analgesics and antiemetics can be really important. You're looking for the urine output. Their BUN and creatinine can also be helpful, and then certainly their vital signs. If they're not able to tolerate oral intake within two days, consider enteral nutrition. And then any intervention that's specific to the cause of pancreatitis. And so what I mean by that is if they have CBD stones, you may need an ERCP. If they're on medications that could be causing acute pancreatitis, you want to discontinue those. And if we try to classify what the severity of acute pancreatitis is, mild acute pancreatitis is the absence of organ failure and no local or systemic complications. Moderately severe acute pancreatitis, there's no organ failure, or there's transient organ failure, meaning less than 48 hours. And then severe acute pancreatitis is persistent organ failure more than 48 hours, and that may have one or more organs involved. Prognostic scoring systems do exist for acute pancreatitis, but they're really tough to use. So a lot of them lack the sensitivity and specificity. They do need time. So if you have to calculate on admission, and then again, 24 hours or 48 hours later, that's two days of having patients in the hospital without having a great prognostic score yet. And they can be of limited predictive value. And so I listed them here, the Ransons, Modified Ransons, Apache 2, CT score, and Harmless pancreatitis score. In severe acute pancreatitis, there are local regional complications like pancreatic necrosis. There can be systemic complications like that SERS response, multi-organ system dysfunction. ICU care is often necessary in severe acute pancreatitis, and that mortality risk is going to rise substantially. And treatment really centers around that excellent supportive care, which includes potentially ICU care. But earlier in the talk when I mentioned that the incidence is rising, and really our outcomes haven't improved much, it's because we don't have too much to do other than that supportive care, that aggressive IV fluid hydration, and then just, you know, trying to give patients analgesics and antiemetics that's needed and monitoring for those complications. And so in this patient, his sitagliptin was discontinued because that is known to potentially cause acute pancreatitis. He was managed with supportive care. He was on the floor the whole time, did not require ICU stay, and rapidly his pain had improved. And so on hospital day two, he was able to resume his oral intake, and then he was discharged home the next day. He did really well for about eight months, and then he had recurrent severe acute epigastric pain, fevers, and chills, and he came to the ED for evaluation at that time. His bilirubin was 3.3. His AST and ALT were both elevated over 200. Alkaline phosphatase was elevated, and his lipase was again over 5,000. And this time his white blood cell count was 22. And so a polling question for everybody. Based on this patient's presentation and labs, what is your immediate concern? Pancreatic necrosis, cholangitis, pseudocyst, diet, and drug use. And the key here is immediate concern. What are we most worried about? Yeah, so cholangitis is our immediate concern. Pancreatic necrosis may develop over time, but the thing that will be potentially the most harmful and require the immediate intervention is that cholangitis. And so how do we diagnose acute cholangitis? Well, you need at least one between fever and shaking, chills, and elevated WBC or CRP. In the setting of cholestasis and in the setting of some evidence of underlying etiology, whether it be a bowel duct stricture or a stone, a biliary stent in place, something has to be there that you could call the cause of it. And so in this patient, we did an MRCP, and he had a seven millimeter filling defect in the distal CBD, which is down in here. And you can see that there's some duct dilatation that actually extends up into his intrahepatic ducts as well. So an ERCP was performed. This is your ERCP scope, and you can see that there's a stone sitting right in there. He had a sphincterotomy, the stone was removed, and then this plastic biliary stent was put in place. This is often done in the setting of removing stones, because if there's some edema after the procedure, you want to make sure you have the stent in place to facilitate that biliary drainage. And then within a few weeks, you can take that stent back out and make sure the duct is nice and clear. He had a cholecystectomy performed during his hospitalization, had an uneventful postoperative course, and was discharged home tolerating his oral diet. He had no residual epigastric abdominal pain. The repeat ERCP was done six weeks later, that biliary stent was removed, and a cholangiogram was performed with no residual CBD stones. I wanted to comment on this timing of cholecystectomy and gallstone pancreatitis. There's been quite a bit of literature out there over the last five to eight years, and a lot of it supports having a cholecystectomy within the same admission. And so one study had said within 24 hours of admission, you're reducing the number of ERCPs, the time to surgery, and the 30-day length of stay. Another study had said that the same admission reduced healthcare costs. Patients with severe acute pancreatitis may not be a candidate for same-day admission cholecystectomy though. And so in that case, you should perform it as soon as you can after the initial incident. And so moving into some potential complications of acute pancreatitis, the most common by far is pancreatic pseudocysts, but you also can get that necrosis of the pancreas or the peripancreatic tissue and multi-organ failure. And this is an example of some pancreatic pseudocysts, kind of this darker gray are the fluid collections. So how do we manage these? You know, if they're asymptomatic, we typically just observe them. You can do follow-up imaging with a contrast enhanced CT scan or an MRI every three to six months, make sure that they're not continuing to get larger in size. If they're symptomatic or if they're rapidly enlarging, or if they're infected, then you want to consider drainage. The most common symptoms with these would be that kind of epigastric fullness or bloating, sometimes nausea and vomiting. If you think about your stomach's kind of like a balloon, and if you have a space occupying pseudocyst sitting there, your stomach can't expand as much. So sometimes they'll complain of early satiety or decreased oral intake as well. Endoscopic pseudocyst drainage can be done when it's needed. So there's the transgastric or transduodenal approach, depending on the location of the cyst, where you can put one or more pigtail stents. There's transpopulary, when you have small cysts that communicate with the main pancreatic duct. And these are actually really successful, so up to 95% success rate. They do recur 10 to 20% of the time, and I think a lot of that has to do with how long you leave the drain in place, if you're CTing it before to make sure that you're removing it, and then if they have recurrent, repeated attacks. And so this is an example of the transgastric. And so you can see that there's a really large pseudocyst that's sitting here. You can imagine that this makes it hard for the person to maintain normal oral intake. And so they had, you can see the wire here, placed within it. This is a pigtail stent. It's going to drain that into the stomach. And so this is after four weeks, and then after nine weeks, and you can see that the stent is still coiled there, but much better. Pancreatic necrosis is lack of perfusion of the pancreas with ischemic necrosis. There's an increased risk of severe complications with this, and you should treat them if they're symptomatic or infected. And so that would be your endoscopic cystogastrostomy and serial debridement, which is your necrosectomy. And so, again, placing a stent from the stomach, typically into that cyst, and then debriding it, sucking out the contacts to the best of your ability, leaving that stent in place to help facilitate drainage. Internal radiology can also put a percutaneous catheter sometimes in these pseudocysts, and occasionally they do require surgery, but I think the majority of them, now that we've had a little bit of a shift in our advanced endoscopy, is being done endoscopically. And so this is an example where you're able to go in and place this catheter. And this is what it can look like, where we can see it draining. And so a question, which of the following can cause recurrent acute pancreatitis? Pancreas divisum, hereditary pancreatitis, autoimmune pancreatitis, or choledocal lithiasis microlithiasis, or all of the above? Perfect, I put in all of the above as we're in our post-lunch coma, but absolutely, all of these are really important reasons. And so I just want to go through each of them briefly. So pancreas divisum is the most common congenital malformation of the pancreas, happens in about 3%. And it's the failure of the dorsal and the ventral pancreatic ducts to fuse. And so you have your dorsal duct here, and instead of it joining, you can see that your ventral duct is separate. The majority of the drainage then is going to go through this dorsal duct, the smaller one. Most often this is asymptomatic, more than 95% of people who have pancreas divisum do not have episodes of pancreatitis. And so if you have somebody who had one episode of acute pancreatitis, and they instantly are found to have pancreas divisum, you don't want to make the mistake of automatically assuming it's the divisum until you've ruled out everything else. And ideally, you want them to have more than one episode before you really blame it on that. If they do have recurrent episodes of pancreatitis, you can do a minor papilla sphincterotomy. And so with that, you're opening up that minor papilla to allow more easily drainage. Hereditary pancreatitis is another thing that's not very common, but important to think about in our differential diagnosis. Most commonly, it's a variant in the PRSS1 gene, and it's autosomal dominant. The SPNK1 and the CFTR genes can also cause hereditary pancreatitis. These are autosomal recessive, so they're just a little bit less common. The important thing to remember about hereditary pancreatitis is that they have a significantly higher risk of developing pancreatic cancer. And so these patients actually have upwards of, you know, 50% chance of pancreatic cancer in their lifetime. And so keeping that in mind, although there are no guidelines that say we should be screening these patients, I think imaging usually is warranted to make sure that we're looking for hopefully early disease if they're going to develop it. The other thing is for patients who really suffer with this and have severe acute recurrent pancreatitis, total pancreatectomy can be considered. And that will help from a recurrent pancreatitis standpoint, as well as reduce the risk of pancreatic cancer. And then autoimmune pancreatitis, they are divided into two types. So type one is when you have your IgG4 positive plasma cells. And so when you go in to take a biopsy of the duodenum, you can stain for this as well. And then your serum IgG4 is typically two times the upper limit of normal. Type two is more of a granulocytic lesion. They don't get that IgG4 positivity. They don't have systemic involvement. This one can be a little bit more challenging to diagnose. And I think more commonly, if you have a high suspicion for it, you'll treat them and see that things improve and that kind of solidifies our diagnosis. And so pancreatic manifestations tend to be pancreatic mass enlargement or prominence on imaging. They can have mild abdominal pain. They may develop pancreatic duct strictures. They could get obstructive jaundice and extra hepatic and intrahepatic strictures as well. We typically will treat these with glucocorticoids. And then a lot of times you'll start that if they get better or if you have a high suspicion for the diagnosis, particularly if you have IgG4 positive staining, you'll put them on immunomodulators for more of a maintenance regimen. And so that can be rituximab, more commonly azathioprine. Once they're on that therapeutic dose of your immunomodulator, a lot of times you can successfully taper off the glucocorticoids. If there are biliary strictures that do not resolve with this therapy, then they may require ERCP to have balloon dilation and management of that stricture. And so this is an example, again, this is our ERCP scope, and there's a really tight stricture here. And so coming up in here, this is the end of the balloon dilator. And then a sensor placed right across that stricture. So this was somebody that we had seen who was on immunomodulator therapy and still just had this persistent, really severe biliary stricture. And so in summary, the incidence of acute pancreatitis is increasing. Management is still quite a challenge. ERCP is indicated for cholangitis, but remember that it doesn't reduce the severity of acute pancreatitis, and it probably doesn't even affect the duration of pancreatitis. CT scan is generally not warranted or helpful within the first 48 hours. Pancreatic scoring systems exist, but they're tedious, they lack sensitivity and specificity, and they have limited predictive value, which is part of what makes it so challenging for us to identify these patients who are going to develop severe courses of acute pancreatitis and be able to manage them appropriately. Early diagnosis, pancreatic rest, IV fluids, and recognition of SIRS are really important concepts.

acute pancreatitis

case-based format

diagnostic tests

management

complications

recurrent acute pancreatitis