Slide 1: It is interesting that when talking to the senior residents pancreatic surgery, they will say this little bit of surgical wisdom: eat when you can, sleep when you can, and do not mess with the pancreas. Although a few of them will use different word than "mess". If you ask Dr. Abontanos, he will say: "The pancreas is like a landmine". Slide 2: Pancreatic Basics: It is a retroperitoneal organ with exocrine and endocrine function. We will review this briefly for the students. One to liters per day, twenty different digestive enzymes, amylase and lipase are secreted in active form. The other enzymes are secreted in inactive form. The endocrine function as from the islets of Langerhans and secretion of multiple hormones including insulin, glycogen, and somatostatin, etc. Slide 3: Pancreatic Anatomy: The head is opposed to the duodenum. The insulate process curves around the superior mesenteric artery and vein. Then neck is anterior to the superior mesenteric artery and vein. The body and tail go up into the left upper quadrant and the spleen is at the tip of the tail of the pancreas. Slide 4: Arterial Anatomy: There is rich arterial incidence. In the celiac trunk it is cephalic in the hepatic arteries as well as cephalic from the superior mesenteric artery. Slide 5: There is extensive rich venous outflow via the splenoportal system. Slide 6: Ductal Anatomy: There are two major ducts. The main duct, Wirsung and the minor duct or accessory duct of Santorini. They do not connect here. That is a congenital abnormality called Pancreas divisum, and the common bile duct and the main duct have a common channel of about 1/2cm in the duodenal wall. Slide 7: Pancreatitis: We are going to start with acute and move on to chronic. We will start with the definition. Slide 8: Acute pancreatitis is defined as a non bacterial inflammation of the pancreas caused by the activation, interstitial liberation and digestion of the gland by its own enzymes. Slide 9: The incidence of acute pancreatitis is about 38 cases per 100,000 people per year and for an unknown reason, the incidence is increasing. While 10 to 25% of cases are estimated to be severe pancreatitis, I think that is probably an over estimate, but some studies do have as high as 25% incidence of severe pancreatitis. The average length of stay in the literature is anywhere from 40 to 226 days. As you can imagine the average cost of the care of those patients is astronomically high. Although that has not been well defined in the literature. The etiology of acute pancreatitis depending on where you practice is either gallstones or alcohol. Here at MCV probably the majority of patients do have alcohol induced acute pancreatitis. Another 40% or so in the literature are gallstones and there is a number of other etiologies that I will briefly mention. Of interest is that only 10 to 15% of large alcohol consumers end up with pancreatitis and those patients usually do not have alcoholic cirrhosis. That is another 10 to 15% of patients who are severe alcohol abusers. In this slide, of note, I will just say that post operative acute pancreatitis has been shown to have the worse ambiguity and mortality of all of the etiologies of pancreatitis. The other etiologies are much less common. Slide 10: The pathogenesis of acute pancreatitis and chronic pancreatitis for that matter are unknown. There are many punitive mechanisms. They include enzymatic digestion of the gland by its own enzymes, duct obstruction that leads to interstitial pancreatic hypertension, duodenal or biliary reflux. Increased pancreatic duct permeability, enzyme, auto activation. And specifically with regards to alcohol, it is not well understood, but it is thought probably to be related to either sphincter spasm, cellular metabolic poison, or the formation of protein plugs in the pancreatic duct that leads to obstruction. There has been some recent progress in hereditary pancreatitis and it is now believed that Type I and Type II hereditary pancreatitis are caused by a failure of inactivation of prematurely activated chymotrypsin. Slide 11: For the students, clinical presentation of acute pancreatitis are severe epigastric pain that radiates to the back associated with nausea and vomiting. There is epigastric and possibly diffuse tenderness. In severe pancreatitis, you can have ascites, hypotension, systemic inflammatory response syndrome. For the students, these are the two most common questions on the wards: what are Cullen's sign which is periumbilical ecchymoses and Grey Turner's sign which is flank ecchymosis. Slide 12: So how do we diagnose acute pancreatitis? History and physical, of course, laboratory analysis, and imaging is needed. Once again for the students, you will be asked this many times on the wards: When the amylase level does not correlate with the severity of acute pancreatitis. I will say you might not hear this from many surgeons, but acute pancreatitis should be considered a diagnosis of exclusion. I say that because about once every three months, we have a patient referred with acute pancreatitis that has actually had a conservative non-operative management of a perforated ulcer or bowel obstruction or appendicitis. You must consider all of the other diagnoses in patients who have pancreatitis. Slide 13: It is important to grade the severity of acute pancreatitis since the spectrum of acute pancreatitis there are two basic classifications: mild or severe. Mild is defined as pancreatic and peripancreatic edema and fat necrosis without gland necrosis. This is commonly referred to as edematous pancreatitis. Severe pancreatitis has extensive pancreatic, peripancreatic necrosis and plus or minus hemorrhage. And this is commonly called necrotizing pancreatitis. Slide 14: The severity is easily graded and by any of a number of grading schemes. The most commonly used is the clinico-biochemical Ranson's criteria. There is also Apache II and bounces are for radiologic grading systems. Slide 15: Ransoms's criteria, as most of you know, are determined in the first 48-hours after admission. The admission values are age, white count, glucose, LDH and SGOT. Forty-eight hours after admission the hematocrit falls, BUN increases, calcium less than 8, PAO2 base deficit and fluid sequestration. Slide 16: Why is this important? Because the treatment and the evaluation of patients who have mild to severe pancreatitis is different. As you can see if you have mild pancreatitis that is characterized by a 0-2 Ransome's criteria, the mortality is only about 2%. Severe pancreatitis is 3 or more Ransome's criteria, you go any where from 15% up to 100%. The overall mortality for acute pancreatitis in the literature is somewhere in the nature of 10 to 35%. That is for severe pancreatitis. Slide 17: Medical management of mild to acute pancreatitis is relatively straight forward. Supportive care is the cornerstone of treatment. Crystalloid buying resuscitation, I can not emphasize this enough. To give you an idea of how much crystalloid we are talking about, if you look at the peritoneal surface area, it is about 1.8 liters square. If the chemical burn from pancreatitis increases the thickness by about 1mm, you will need to have eighteen liters of fluid to resuscitate the patient. Pain control also is very important. Radiologic evaluation is minimal. I will talk about that in a second. Nutritional support in mild acute pancreatitis essentially consists of making the patient NPO and instituting a feeding trial when clinically improved. Of course, it is important to observe the patients for complications or worsening pancreatitis. If the patient is an alcoholic, he should have a substance abuse consult as well. Slide 18: For mild acute pancreatitis, you need to obtain an ultrasound as indicated to evaluate for gallstones. If the have known gallstones, then you probably do not need to get an ultrasound. You do not need to have a CT in mild acute pancreatitis unless you have a unclear diagnosis, you have a persistent illness for two or three days or you suspect a complication. CAT scan is grossly overused in patients with mild acute pancreatitis. Slide 19: Severe acute pancreatitis is a terrible disease. The most important thing in reading literature and this is agreed by pretty much every author to refer the patient to a multi-disciplinary center that specializes in the care of these patients. After that, institute appropriate supportive therapy and then prepare the patient and the family for a very long complicated expensive hospital stay that could end up with the death of the patient. As we mentioned, the mortality is any where from 10 to 35%. Slide 20: Macro managing the severe acute pancreatitis begins with supportive care and move on with appropriate radiologic evaluation. Nutritional support has had some recent advances. Patients with severe acute pancreatitis should receive prophylactic antibiotics, which we will talk about. An ERCP is performed only as indicated. There have been some recent studies and there is Japanese and European literature which suggest that protein ace inhibitors and platelet activating factor antagonists might be helpful in lessening the severity of morbidity and mortality of acute pancreatitis. Slide 21: Supportive care, once again, begins with volume resuscitation. The patient should remain NPO and have an NG tube inserted as necessary, Foley catheter should be inserted to monitor fluid resuscitation. Invasive monitoring is used as necessary to guide resuscitation. I will say that if you do not have a Swan, you should not give Lasix. There is a tendency that these patients receive Larix when they start to go into renal failure with some of the less educated providers. It is very important: No Swan - No Lasix. Intubation is also used if necessary. Interestingly about 50% of patients with acute pancreatitis will develop pulmonary complications. The most common cause of death in the first week of severe acute pancreatitis is actually respiratory failure. Slide 22: The radiologic evaluation of severe acute pancreatitis begins with a CT scan. An initial CT on presentation and a repeat CT if you suspect a complication. CT guided fluid aspirations are obviously very helpful in patients that you suspect have infected pancreatic necrosis. If you do not know if gallstones are involved, then an ultrasound would be indicated as well. Slide 23: Nutritional support has had some progress recently. Enteral alimentation is now preferred over TPN in severe acute pancreatitis. The formulation is usually a low fat alimental or a small peptide formulate that is fed via the jejunum. In randomized prospective trials, enthrall feeding has been at least as safe and well tolerated as TPN. It did not significantly stimulate the pancreas. It decreased the stress and inflammatory response and possibly decreases bacterial translocation and is definitely more cost effective. TPN, however, is still useful in patients who do have obstruction or ileus. One of the other benefits is that you can rapidly obtain vascular access and reach your nutritional goals. Slide 24: Antibiotic prophylaxis. There is a recent review article by Powell, et al, in the British Journal of Surgery in 1998. In a Medline Review from 1990-1997, they looked at four randomized prospective trials. While they found decreased pancreatic and extra pancreatic infection rates in patients that received prophylactic antibiotics, there was no significant decrease in mortality, although the ends were small. They did not perform an analysis as the different trials utilized different antibiotic regimens. But based on this and standard clinical practice over the years, the current recommendations are patients who have severe acute pancreatitis over a long period of time, and that is about one month. The reason why a long duration of administration is utilized is because the pancreatic abscess ends its peak in about three weeks after the onset of the disease. They also emphasize that a large randomized blinded trials are needed. The other thing that is one the horizon is selective gut decontamination that also looks to be promising. Slide 25: ERCP is not indicated in mild acute pancreatitis for all patients. With mild acute pancreatitis, a laproscopic cholecystectomy with intra operative cholangiogram is more cost effective, at least here at MCV. However, in severe acute pancreatitis, if you have an impacted ampullary stone, then you should perform an ERCP and a stone extraction. An impacted ampullary stone is evidenced by documented gallstones, elevated bilirubin and alkaline phosphatase, and a clinical course that does not improve in twenty-four hours. If you follow the selection criteria, and ERCP will decrease complication rate. It is unclear whether or not the improvement and complication rate is related to the resolution of pancreatitis or the resolution of cholangeitis. Slide 26: So when do we operate on acute pancreatitis? There are three indications: unclear diagnosis, gallstone pancreatitis, and local complications. Slide 27: Once again, I will re-emphasize the diagnosis unclear equals exploratory laparotomy. Do not delay operation in patients who have acute abdomens. Slide 28: There is a study looking at the symptom duration, hours versus the mortality rate and secondary peritonitis. That is 0-6 hours and 9% mortality if you get up to three days of symptom duration, the mortality approaches approximately 50%. Slide 29: Surgical intervention in gallstone pancreatitis. Mild acute pancreatitis as already mentioned, requires a cholecystectomy with cholangiogram after the resolution of acute symptoms during that admission. In severe acute pancreatitis, you do an ERCP as indicated and after the resolution of acute symptoms, you perform a cholecystectomy. Slide 30: Complications of acute pancreatitis. By far the most common complication is infected pancreatic necrosis. Ischemic necrosis of adjacent viscera is also an indication. There is a debate in the literature as to whether or not worsening clinical condition despite maximal medical treatment is an indication. Of note, the mortality is equal and the morbidity is greater with surgical intervention and no other indication. But, operation obviously will help patients who have undiagnosed infective necrosis. The determination of infective necrosis or sterile necrosis is a very difficult thing to determine and that is very difficult at best. Other things that need to be treated via surgery are pancreatic abscess, although pseudocysts that are symptomatic are complicated. Slide 31: Infective pancreatic necrosis has a 100% mortality if it is not resected. The most common means of necrosectomy here at MCV is serial debridement. We use temporary abdominal closure with a ventral fascial closure with closed drainage. There is a recent study by Hunter, et al, in the Annals of Surgery, with that technique there is about a 72% organ failure rate, a 12% mortality rate, and a likely stay of about 54 days. If you look at those numbers, those are actually very good in comparison with the rest of the literature. We occasionally use retro peritoneal marsupialization with open packing of the lesser sac. We essentially never used single debridement and closed drainage. Of course, it is obviously important to establish enthral access at the time of the debridement, that is a jejunostomy plus or minus a gastrostomy tube. Slide 32: We will move on with surgical intervention for pancreatic abscesses and pseudo cysts. Abscesses peak incidence of onset are about three to four weeks after the onset of acute pancreatitis. There is about a 20% mortality. External drainage is best performed operatively. It can be performed percutaneous only if the fluid is thin. But a pseudocyst is not a true cyst. It has no epithelial lining. The walls of a pseudocyst are inflammatory tissue and surrounding organs, and there are multiple techniques available if drainage is indicated. Slide 33: The indications for pancreatic pseudocyst drainage have changed. It is not longer 6cm at six weeks which was the old surgical dictum. Lastly, pseudo cysts require drainage if they are persistent symptoms: they are mature, they have failed conservative management, or if they develop complications. Slide 34: Endoscopic management of pancreatic pseudo cysts which was reviewed by Beckingham et al in the British Journal of Surgery in 1997. If you look at the different drainage techniques, transpapillary drainage, endoscopic cyst gastrostomy, endoscopic cyst duodenostomy, percutaneous catheter drainage and internal surgical drainage. Except for the surgical drainage, which were very old studies - I do not know why they pick these studies, probably because of the large number. The remainder of these techniques, the studies and all literature are very small studies. The long term success rate of, as you can see, endoscopic cyst gastrostomy is only about 64% successful. The recurrence rate is high with endoscopic cyst gastrostomy. I know of one patient in town who died from hemorrhage during an endoscopic cyst gastrostomy. Hemorrhage is a significant part of the morbidity here. Endoscopic cyst duodenostomy is fairly good with a success rate, very low recurrence rate, and that one death was not related to drainage of the pseudocyst. Catheter drainage has a poor success rate in general with a high visualization of recurrence rate. Slide 35: Conclusions: Pseudocyst drainage techniques. There are no randomized prospective studies. Case reports and small studies provide user techniques that have not been rigorously investigated. There has been an unfortunately recent trend towards long out-patient treatment via percutaneous and endoscopic drainage techniques. The most important thing that I can say is that randomized trials are needed in the care of these patients and should be done in multi-disciplinary centers where a gastroenterologist or radiologist and surgeon work in conjunction with each other. Slide 36: We are now going to move on to chronic pancreatitis. Chronic pancreatitis is defined as an inflammatory disease of the pancreas characterized by continuous and/or episodic abdominal pain and progressive loss of endocrine and exocrine function. Slide 37: The incidence and cost of chronic pancreatitis. The incidence is five to ten cases per 100,000 people per year and the prevalence is about 27 cases per 100,000. Once again the cost has not been well delineated, but it is very high. Slide 38: The etiology of chronic pancreatitis. In most centers it is alcohol, alcohol, alcohol and alcohol. Idiopathic pancreatitis in some studies actually accounts for up to 40% of cases. There is a number of other etiologies include acquired strictures, neoplasm, chronic hypercalcemia and cystic fibrosis. Slide 39: The pathogenesis we have already reviewed that for acute pancreatitis. I will not review that again. Slide 40: Clinical presentation is a tirade of current or contracted abdominal pain with a possible diabetes and steatorrhea. Radiologic presentation: pancreatic calcifications and pancreatic duct abnormalities are commonly called the "chain of lakes". It is a dilated and/or strictured duct. Slide 41: MRCP has moved to the forefront of radiologic evaluation of chronic pancreatitis because of its ability to image the ducts, the pancreatic parenchyma and the vessels. Although at most non-tertiary care centers, computerized tomography is still the main stay of imaging. ERCP and EUS are important with regards to tissue diagnosis, but have moved out of the diagnostic and more into the therapeutic realm. Slide 42: Treatment of chronic pancreatitis. Once again if you look at the literature, one recurrent thing throughout the literature is referring the patient to a multi-disciplinary center. Maximize medical management. You only need to operate if you have complications that refractory to medical management. And with regards to selection of procedure, I would select a procedure that addresses all of the pathology. In general, drainage procedures are less morbid than resection. Slide 43: The complications of chronic pancreatitis. Do we need to treat pain? Exocrine and endocrine insufficiency. Duodenal obstruction, common bile duct obstruction, pancreatic duct obstruction or leak, splenic vein thrombosis, carcinoma. Medical management of complications of acute pancreatitis begins with pain management. Pain is the most common complication that will bring the patient to the hospital. The one thing that we utilize at MCV which I think is crucially important, is the patient care contract. They agree of the cessation of alcohol intake and obtain narcotics only from the clinic. This does invest the patient in their own care and makes them somewhat responsible for the cessation of alcohol and narcotic use. Interestingly, about 50% of patients who stopped drinking alcohol have substantial pain relief. Substance abuse is a key part of alcohol cessation as well. Narcotics are used as necessary and generally are moved from a nonsteroidal to weak PRN narcotics to stronger long duration narcotics. Most of the search for literature will recommend that you refer the patient before they are addicted because the results of surgical intervention are generally better if they are not addicted to narcotics. Exocrine and endocrine insufficiency is treated with high carbohydrate low-fat diet and there is a question as to whether or not enzyme supplementation will help with pain. It probably does help with malabsorption. And blood sugar is controlled with medicines as necessary. If the patient develops duodenal, biliary or pancreatic duct obstruction, you should try a trial of non-operative supportive therapy before you surgically intervene. Slide 44: Very frequently asked questions as what do you do with splenic vein thrombosis in chronic pancreatitis? There is a nice study of the natural history of splenic vein thrombosis in chronic pancreatitis that was published by Bernades, et al, in 1992. The overall incidence in literature of splenic vein thrombosis in chronic pancreatitis is about 5 to 55%. The average is around 20%. They had a study of about 226 patients with chronic pancreatitis that they followed for a fairly long period of time. They found splenoportal vein obstruction in only in 35 of those 226 patients. Only 6 of 35 patients developed esophageal gastric varices and only one of those patients developed variceal bleeding. Therefore, you do not need to operate on those patients that have splenic vein thrombosis. The indications for splenectomy are gastric varices bleeding or complication of pancreatitis that requires an operation that is associated with splenic vein thrombosis and varices. Slide 45: Although it is controversial, recent evidence suggests that there is a two to three-fold increase and the risk of carcinoma in chronic pancreatitis. Because of that and also if you have pancreatic mass, a dominant mass in a patient you are going to operate on, you should resect the mass if at all possible. As unresected pancreatic carcinoma, as we know, results in the death of the patient. If you are going to do a drainage procedure, you should send samples of the pancreas or pseudocyst for evaluation at the time of the procedure. Slide 46: Surgical management of chronic pancreatitis. The major indication is chronic pain and that is refractory to medical management. Also other indications include duodenal or biliary duct obstruction, pancreatic pseudo cyst or ascites with a pseudocyst as we already mentioned, or mass. I think that it is important to select a procedure that addresses all pathology including biliary, pancreatic, duodenal, and splenic vein. As mentioned previously, drainage in general has more morbidity than resection and that is for head disease. Frey or Begar procedure are, in general, less morbid than a Whipple and a Whipple has anywhere from a 40 to 50% post operative morbidity as compared to 20% morbidity with the Frye or Begar. But the difference between the two in the post operative morbidity is mainly related to delayed gastric emptying with regards to pyloric scarring with the procedure. Slide 47: Once again the selected procedure that best treats the constellation of pathology. The most common procedures include a longitudinal pancreatojejunostomy, Frey, Begar, and Whipple and distal pancreatectomy are pretty much the most common procedures performed. With regards to a basic scheme for selection of an operation: If you have parenchymal disease and ductal dilatation that is located in the head only, Whipple is a reasonable choice. If it is in the head of the body, Frye is probably the reasonable choice. If it is in the body and tail only, then longitudinal pancreatojejunostomy or distal pancreatectomy is reasonable. If you have no ductal dilatation, interestingly in the past, we used to say that the patient was not a surgical candidate. There is a recent study that I will go over in a moment that suggests that a V-shaped ventral incision of the pancreas can be beneficial for these patients. Of course if you have a dominant mass, you resect it. If you have splenic vein thrombosis or varices, you add a splenectomy. If you have a lower stricture, you need to either do a choledochostomy or consider Whipple. If you have cholelithiasis, you should take the gallbladder out. Slide 48: What can you tell patients to expect after surgical intervention for chronic pancreatitis? There is a paper that was recently published in the Journal of Gastrointestinal Surgery in 1998. The amount of morbidity after operations for chronic pancreatitis is up to 50%. Major morbidity such as bleeding and pancreatic leaks is up to 5% for each of these complications. Mortality is less than 5%. The average length of stay is between one and a half to two weeks. This is longer for Whipple procedure. Pain relief is the sustained in 85% of patients in the three to five year time frame. Another 10 to 15% of patients will develop diabetes in the decade after surgery. They also mention that stenting with lithotripsy neurolysis, thoracic splenoseptomy, etc. should be considered short-term therapy. And once again, surgery should preferably be performed in specialized centers. Slide 49: This is a pictorial review of the history of surgery for chronic pancreatitis and this is mainly for the students. There are a couple of unusual procedures that we perform. A fair number of people in the audience probably do not know about. It began with Mallet Guy in 1942 as a distal pancreatectomy. Actually this was not a splenic preserving distal pancreatectomy, but was a distal pancreatectomy. Slide 50: We moved up to Duval in 1954 where they did a caudal pancreatojejunostomy. Cut off the tip of the pancreas and the spleen and then bring the lower end up and do an end-to-end anastomosis. As you can imagine, this did not do very well with regards to the rest of the pancreas. Slide 51: Puestow Gillesby in 1958 introduced a longitudinal pancreatic- odocotomy with pancreatic invagination into the jejunum. As you can see, you open up the duct longitudinally, you cut off the tip of the pancreas and take out the spleen, Slide 52: and then you bring the lower end up and invaginate the pancreas into jejunum. Slide 53: That was subsequently improved with the modified Puestow Gillesby or the longitudinal pancreatojejunostomy or lateral pancreatic jejunostomy. Partington and Rochelle in 1960. And with this you do the same thing. You open up the back but you just anastomose the jejunum to the pancreas. That is the most commonly performed operation, by the way. Slide 54: Pancreaticoduodenectomy was introduced for chronic pancreatitis by Whipple in 1964. Take out the head of the pancreas, the duodenum, and then you anastomose the jejunum to the pancreas, the bile duct and the stomach in any of a number of different reconstructions, but it looks something like that. Slide 55: Total pancreatectomy was advocated by Warren in 1966 for chronic pancreatitis. The whole pancreas is gone and the duodenum and you are left with connecting the jejunum to the stomach and to the common bile duct so that it looks something like that. That is not very commonly performed as you can imagine because of the complications related to brittle diabetes. Slide 56: The pylorus preserving pancreatic duodenectomy was reintroduced by Traverso and Longmire in 1978 for chronic pancreatitis. You take the pancreatic head and the part of the duodenum. Slide 57: It is reconnected in the following configuration. That is fairly commonly performed. Slide 58: The Beger Procedure. Beger introduced his duodenal preserving pancreatic head resection in 1980. You take out the head of the pancreas but leave some of the pancreatic tissue about the duodenum and then you anastomose the pancreas to the jejunum on two separate places. You can also open it the pancreatic duct and jejunum if you need to as well. Slide 59: The reconstruction looks something like this. This is utilized for patients with a component of head disease. Slide 60: Frye introduced a variation of the longitudinal pancreatojejunostomy in 1987. He added a local pancreatic head incision. You basically, as Dr. Sugerman would say, take a nine iron wedge out of the head of the pancreas. That drains the ducts in the head in addition to the minor duct, the annular duct to the anci. The pain relief for that operation is very good. This is one of the more commonly used procedures here at MCV. Slide 61: There is the ongoing area of reconstruction. Slide 62: As I mentioned the longitudinal ventral pancreatectomy with pancreatojejunostomy was recently advocated by Izbicki, et al, as recently as 1998. This is for small duct disease. There is no duct to open. What you do is basically take a "V" shaped wedge out of the entire length of the pancreas and then you connect it to the jejunum in the standard fashion. Slide 63: This is a departure for surgeons in the last several years. I am just going to briefly go over this study. In the prospective study, about 13 patients with a median follow-up of about 30 months. The maximum duct size was about 2mm. Although if you read the whole paper, there is one patient who had a pseudocyst. I do not know how many other patients had a concomitant disease. They collected cytometric, exocrine and endocrine data. Results were fairly impressive. Morbidity of 15% and 0% mortality. Morbidity was temporary and this was related to a bile leak in a transient pancreatic fistula. There was complete pain relief. No narcotic use in 92% of the patients. The exocrine and endocrine function stayed stable. While this was a small study, with relatively short term follow up, the results should at least be considered for further investigation. It potentially helped patients for the firs time that have small duct disease. Slide 64: We are going to conclude this with a couple more of brief slides describing our MCV Pancreatitis Center which is a specialized multi-disciplinary center that specializes in the care of these complex patients. Reductions in patient care teaching. Research in the center and it is outcome based medical care. We have a Pancreatitis Clinical Path that has been shown that we have maintained the quality of the care of these patients and we have decreased the cost of admission by about $1000 per patient admission. I believe that every patient has acute severe or chronic pancreatitis should be referred to a specialized center. The surgical route may need to be changed just a little bit. Eat when you can, sleep when you can, and let the experts and specialized multi-disciplinary centers mess with the pancreas. Thank you very much!