During this 20-25 minute pre-recorded lecture, Dr. Nicholas Hoerter discusses the topic of acute pancreatitis. This in-depth review will provide an update on this topic for your clinical practice as well as supplement your learning for the ABIM Gastroenterology and Hepatology boards. CME pre-requiste of live Q & A webinar, 8th Annual Mount Sinai Intensive Board Review in Gastroenterology & Hepatology on Sept 29.
Hello. My name is Nick herder. I'm the advanced endoscopy fellow at Mount Sinai and today I'm going to be speaking about acute pancreatitis First some objectives, The objectives for this talk are to establish a definition of acute pancreatitis and classification. Understand the role of fluids and nutrition in acute pancreatitis, explore the diagnosis and management of late complications of acute pancreatitis and describe the risk factors and prevention strategies for post your city pancreatitis first a definition. So the definition of acute pancreatitis requires two out of three criteria. The first is laboratory which is elevated serum amylase or light based greater than three times the upper limit of normal. The next is clinical which is typical epic gastric pain, severe rating to the back, often in a band like fashion with nausea, vomiting and the third is imaging criteria pancreatitis. It's important to note that imaging is not required for diagnosis. It's most helpful when the clinical scenario is unclear. It's also important to note that the degree of enzyme elevation does not correlate with severity and these enzymes should not be trended throughout the course. There are also other considerations for elevated amylase and light base that are unrelated to pancreatitis. So if the clinical picture doesn't fit, there may be another cause. Now we're going to talk about causes and classification of pancreatitis. The two most common cause is far and away of acute pancreatitis are gall, stone and alcohol related called pancreatitis. 20% of cases are from a smattering of other things. Most importantly, drugs post ERCP autoimmune which can sometimes make pancreatic cancer and of course cancer itself, which can mimic acute pancreatitis or cause acute pancreatitis. There's also 10% of cases that are idiopathic and we never find a clear cost. Now we're going to talk about the classification of pancreatitis, which is defined by the revised Atlanta classification as of 2012. There are two main types interstitial and necrotizing. The phases are early and late. And uh we can also define the severity, which we will talk about. The two main types of pancreatitis are interstitial, which is inflammation and edema of the pancreas and accounts for 90% of acute pancreatitis and is usually more mild with a lower mortality. In this image, you can see a contrast enhanced CT with enhancing pancreatic tissue. That's the key for interstitial pancreatitis in necrotizing pancreatitis. Uh there is necrosis of the pancreatic tissue. This is more rare. It's 10% of acute pancreatitis and it's more severe with a higher mortality. And in contrast to the enhancing pancreas tissue on the left in the image on the right where the stars are, you can see there is non enhancement of the pancreatic tissue, which signifies necrosis and lack of blood flow severity is defined here mild pancreatitis is not associated with organ failure, moderate pancreatitis is associated with transient organ failure or local or systemic complications and severe pancreatitis is defined by persistent organ failure. Organ failure being defined by hypoxia hypertension or renal failure. Obviously there's a time element and it may become clear over the 1st 48 hours whether the patient has moderately severe or severe pancreatitis. The reason we use these criteria is because they directly correlate with mortality need for I see you and length of stay. You can see that uh in this large retrospective study there's also a correlation between severity and likelihood of necrosis. Now for a case presentation case one is a 57 year old female presenting to the E. D. With 12 hours of severe epic gastric pain, fever and nausea. On exam she's federal and technique arctic. Her labs are notable for Lucas psychosis, elevated hematocrit, elevated S. T. A. L. T. And alec fast and a light base of 6300 an abdominal ultrasound. She has gall stones and a CBD normal at five millimeters. Question one is which of the following will most likely improve this patient's outcome A. E. R. C. P. B imaging with M. R. I. C. Aggressive fluid resuscitation. D. Empirical antibiotics or E imaging with C. T. And the answer is see aggressive I. V. Fluid resuscitation and we're gonna talk more about that. So we're going to go through initial pancreatitis management. The first point is to note that early resuscitation improves outcomes in this retrospective study, patients were classified as receiving early or late resuscitation as defined by receiving more than one third of their total fluid over the 1st 72 hours within the 1st 24 hours and you can see clearly there is a decrease in Sir's over the 1st 72 hours in the early resuscitation group. Studies have also shown that LR. Is better than normal saline for resuscitation in acute pancreatitis. This was a small randomized clinical trial and the patients who got lactaid ringers had decreased rates of serves decreased acidosis and decreased crp Another important point is a marker of severity and can also be used to track fluid resuscitation is B. U. N. Uh In this retrospective study with more than 6000 patients, patients who had higher Bunn had higher mortality. And you can also see on the right that although we often use hemoglobin uh as a marker of severity, it did not correlate in this study. Well with mortality goals for resuscitation include a rate of 250 to 500 animals per hour in the 1st 12 to 24 hours. Often this is given as a bullet of a leader or two up front and then 3 to 5 millimeters per kig per hour For the 1st 12 to 24 hours. The type of fluid again, LR. Is better than N. S. And it's thought to be more ph balanced and more electrolytes balanced. The goals of fluid resuscitation should be to decrease the U. N. And hematocrit and also stabilize vital signs and you're not but a brief note about ERCP and gallstone pancreatitis. This is a commonly debated topic but essentially there is not a role for ERCP and gallstone pancreatitis. In the absence of cholangitis. If the patient has cholangitis they should get an urgent ERCP. Uh There's some conflicting data of ERCP in the setting of ongoing biliary obstruction or severe pancreatitis. These could be evaluated on a case by case basis but in general would differ ERCP in these cases. The reasoning for this is that generally gallstone pancreatitis is caused by small stones that impacted the umbrella and impact long enough to initiate the cascade of pancreatitis. But they're also small enough to pass on their own. So they do not always require removal with the R. C. P. Now for question two regarding nutrition and our gallstone pancreatitis patient which of the following is most appropriate. A. Is to start oral feedings with a clear liquid diet. B is to start feedings after light pace is normalized and the pain is resolved. See is to start a low fat diet after nausea and vomiting resolved and pain is decreased. D. Is nasal vaginal delivery of feeds immediately and E. Is TPM after seven days. And the answer is C regarding nutrition acute pancreatitis in mild cases it's appropriate to start oral feedings as soon as the patient feels hungry. Uh nausea, vomiting is decreasing. Pain is decreasing. You can sort of guided by the patient's clinical status and you do not have to go through a progression from clear liquids on you can start straight with a low fat diet in severe pancreatitis, Central nutrition has been shown to prevent infectious complications and is preferred to parent oral nutrition. Uh As we will also discuss nasal gastric and nasa Juno feedings are both acceptable regarding the question of internal nutrition versus TPN. There is a clear benefit to internal nutrition. This is a large Cochrane review in which mortality, multi organ failure and systemic infection were all clearly reduced with internal nutrition. The thought being that internal nutrition maintains that gut barrier prevents bacterial translocation in these sick patients regarding the question of nasal gastric versus nasal regional feeding. Uh you may think that logically it makes more sense to use nasal regional feeding which bypasses the pancreas and won't stimulate further pancreatic enzyme release. But ultimately probably the pancreas when it's inflamed or especially necrotic, is not really responding to feeds anyways. And in uh meta analysis, there was no real difference between nasal gastric or nasal original feeding in terms of pain, diarrhea, um intolerance or need for TPN and the major societies say that nasal gastric is an acceptable alternative to NATO Journal. Uh I would say in most cases we start with nasal gastric feeding and then if the patient doesn't tolerate because of delayed gastric emptying or it doesn't seem like they're improving. Then we would consider placing a NATO generals in that case. Now for case presentation to case two is a 39 year old male with a history of alcohol induced pancreatitis who's admitted with epic gastric pain after drinking heavily on physical exam. He is federal uncomfortable with epic gastric tenderness On labs. He has mild S. T. A. L. T. Elevation, mild at false elevation like pace of 1700 elevated B. U. N. And relatively normal cbC. This is his imaging which you can see a contrast enhancing pancreas with surrounding that stranding and perry pancreatic fluid indicative of interstitial pancreatitis, which the following be the most appropriate next step in this patient's management. And the question here is regarding the perry pancreatic fluid. So should we do a. F. N. A. For gram stain? Perform us guided drainage, perform ERCP with pancreatic stenting. Stay with conservative management or consider open surgical debridement. And the answer is conservative management. And we are going to discuss local complications of pancreatitis. So the revised Atlanta criteria basically break down local complications of acute pancreatitis based on the type of pancreatitis, interstitial or necrotic. And then the phase of the disease here there early or late based on 34 weeks or post four weeks. So in the case of interstitial pancreatitis, the early local complication is an acute parry pancreatic fluid collection and over time this may resolve or after four weeks it may develop into a contained fluid collection uh with a well defined rim. As you can see in the imaging here called a pancreatic pseudo cyst. In the case of necrotizing pancreatitis. An early fluid collection is called an acute necrotic collection. And again over time it may resort or after four weeks it may develop into walled off necrosis and we will go through each of these in turn, this is an example of an acute pancreatic fluid collection, which is what our patient had. This is an early complication of interstitial pancreatitis. It is essentially a collection of enzyme rich pancreatic juice and it results from pancreatic inflammation, potentially rupture of one of the side branches. And it's fairly common in acute pancreatitis management is almost always conservative. They usually remain sterile because they're not necrotic and they regress spontaneously over time. If they do not regress they can develop into pancreatic pseudo cysts. These are cystic fluid collections with a well defined wall and no solid material. The path of physiology is that they arise from disruption of the pancreatic duct and they don't necessarily need to be drained. The only cases that require drainage are if the patient has systemic problems from the fluid collection including pain, uh infection, early satiety weight loss, evidence of frank gastric outlet obstruction or biliary obstruction and in these cases endoscopic cyst gastronomy is comparable to surgery and has a decreased length of stay and I would say both centers at this point have uh converted to using endoscopic sis gastronomy for these cases an acute necrotic collection is the early complication of necrotizing pancreatitis is a collection containing fluid and solid material. It arises from the necrosis of the pancreas or the surrounding tissues early on. It may look the same as an acute perry pancreatic fluid collection. Um And it develops in about a third of patients with pancreatic necrosis. Management depends on whether or not the fluid collection is infected. If it's sterile, it can be managed conservatively and may resolve on its own if there's evidence of infection that NPR's antibiotics are appropriate. This does not require aspiration to determine if the patient is acting clinically infected, it's appropriate to start antibiotics without aspiration walled off necrosis is the late complication of necrotizing pancreatitis. It's a collection containing fluid and solid material and similar to suit assist. It doesn't necessarily needs to be drained, but if it results in gastric outlet obstruction, biliary obstruction. Uh If the patient is just not getting better over time, not eating, not losing weight or losing weight. Uh Or they have evidence of disconnected duck syndrome than these would be indications for drainage. Societal guidelines recommend per cutaneous or endoscopic drainage prior to surgery because they have produced complications and surgical microcephaly can be avoided in up to half of cases with per cutaneous drainage alone. If surgery is necessary, a minimally invasive approach is preferred and many of these cases are complex require multiple multidisciplinary discussion between G. I. I. R. And surgery at an experience center. Next case presentation. three is a 27 year old female with a history of obesity. Presenting with right upper quadrant abdominal pain and jaundice for one week she's found to have colds cystitis with political with ISIS and undergoes uncomplicated ERCP with sphincter academy and stone extraction and post procedurally develops worsening severe abdominal pain, nausea, vomiting. On exam she has epic gastric tenderness, No jaundice her labs pre procedurally she has an elevated tee billy of five elevated alphas S. T. A. L. T. And Lucas psychosis. But a relatively normal light base. Post procedurally her light base jumps up to 31 75. Her LFTs are and Lucas psychosis are improving. And on imaging she has haziness of the pancreatic paranormal with perry pancreatic fat stranding, no new peritoneum and ongoing evidence of cola cystitis. So essentially this patient has post ERCP pancreatitis. The question is which the following places this patient at higher risk for having developed, proposed to be reserved pancreatitis a elevated bilirubin. Be female gender. See no prior history of pancreatitis or de Luca psychosis. The answer is female gender and now we're going to discuss post ERCP pancreatitis risk factors and prevention strategies. So the risk factors for post ERCP pancreatitis can be divided into patient related and procedure related. The patient related risk factors are suspected sphincter body dysfunction. Prior post here. Cp pancreatitis. Normal billy Rubin, young age. Female gender and recurrent pancreatitis. The procedure related risk factors are difficult calculation performing a pre cut sphincter artemis, dilating and intact Hillary's victor ample ectomy pancreatic duct injections and pancreatic sphincters. Sodomy. There are several strategies for reducing post years of pancreatitis including pancreatic stents, rectal insets and aggressive fluids. And we're going to go through each in turn first pancreatic duct stenting. In this large meta analysis there is a clear benefit in both preventing mild moderate pancreatitis and severe pancreatitis and overall prevention of pancreatitis. The reason pancreatic extents work is because papillary trauma from cancellation causes edema of the pd orifice. The edema increases doctor pressures and that results in post ERCP pancreatitis. The stent essentially just holds open the orifice which decreases the pressure and reduces the chance of post your speed. Pancreatitis in general use is limited to high risk patients because the stent placement itself is not without risk. The complications of stent placement results in duck perforation or duct strictures. And so again we only use these in really high high risk patients regarding rectal into medicine. There is also a meta analysis showing that this clearly reduces the incidence of pancreatitis, interestingly. There have been studies using oral and sets and they are not effective for reducing post ERCP banker data. So only the rectal version has been shown to work and universal prophylaxis is somewhat debated. The european society. Endoscopy society recommends into medicine routinely for all your cps. The S. G. Uh recommends into medicine for high risk patients and suggests use an average risk patients I would say at this point because the risk of complications from a single dose of recommended medicine are so low uh that we essentially use this in all cases unless there's an obvious country indication such as allergy or renal failure. The next prevention strategy is peri procedural fluids. And in this randomized trial patients were randomized to standard hydration versus vigorous hydration, and the patients who received more hydration clearly had lower risk of post ERCP pancreatitis, lower risk of having severe pancreatitis. In summary, we discussed the revised atlantic classification of pancreatitis. We discussed that early fluid resuscitation clearly improves outcomes and natural nutrition is superior to TPM. We discussed the various early and late local complications of acute pancreatitis and we discussed risk factors and prevention strategies for post ERCP pancreatitis. Thank you. Mhm.
