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Endoscopic treatment of pancreatic pseudocysts
ERCP-PANCREAS 549
551
ENDOSCOPIC TREATMENT OF PANCREATIC PSEUDOCYSTS. ED Libera JR, ES Siqueira, MRS Rohr, EP Maceclo, AP Ferrari, Endoscopy Unit, Division of Gastroenterology, UNIFESP - Escola Paulista de Medicina, S~o Pauio Brazil. Pancreatic pseudocysts have been successfully treated by endoscopic drainage (cystogastrostomy, cystoduodenostomy and transpapiltaw). We report our experience with endoscopic therapy of pancreatic pseudocysts. From July/94 to November/96, 27 patients with pancreatic pseudocysts ware referred to ERCP because of persistent pain and/or jaudice. In 6127 (22%) endoscopic therapy was not perfomed: pancreatic stenosis could not be crossed (3), there was no indentation of gastric or duodenal wall (2) and a B-II gastrectomy prevented access to the papilla (1). 21 patients, malelfemale ratio 18/3, mean age 36 years (range 24-64 years), 29 pseudocysts ware treated with cystogastrostomy (8), cystoduodenostomy (5) and transpapillary drainage (12). Etiology was: alcoholic chronic pancreatitis (17), blunt abdominal trauma (2) or surgical trauma (2). Pseudocysts mean size was 7,64 cm (range 3,5-20 cm) and they ware located in the head (10), body (14) and tail (5) of the pancreas. Complications were present in 8/27 patients: fever (1), asymptomatic pneumoperitoneum (1), bleeding (3), stent proximal migration (1), perforation (1) and pancraatitis (1). The patient with perforation required surgery, while all other complications ware minor and managed medically and/or endoscopically. There was no mortality. Mean follow up was 225 days (range 30-480 days) and mean stent period was 76 days for transpapillary stents, 41 days for cystogastrostomy and 40 days for cystoduodenostomy. Clinical improvement and pseudocysts resolution ocurred in 19/21 (90%): 15 are asymptomatic and 4 are taking small doses of analgesics. In 2 patients that persisted with pain, sugery was performed. We concluded that endoscopic therapy of pancreatic pseudocysts is a safe procedure, resulting in clinical improvement in most of the patients and recurrence is uncommon in the first year.
POST ERCP PANCREATITIS: DOES ACINARIZATION OR REPEATED PANCREATIC DUCT (PD) INJECTIONS INCREASE THE RISK - A PROSPECTIVE STUDY. NE Lobe, B Dahrnan, JE Geenen, WJ Hogan, MJ Schmalz, MF Catalano, GK Johnson, DJ Gecnen. St. Luke's Medical Center, Pancreatic Biliary Center, Milwaukee, Wisconsin. The most frequent complication of ERCP is pancreatitis occurring in 310% of pts. Potential risks associated with post ERCP pancreatitis are the number of PD injections and acinarization of the parenchyma. AIM: To determine whether the number of PD injections or parenchymal acinarization increases the risk of post ERCP pancreatitis. METHODS: We prospectively evaluated 330 consecutive pts undergoing both diagnostic and therapeutic ERCP (119 male, 211 female; average age 50.8 years). PD injections were not performed in 81 pts and these were excluded as were 53 pts with chronic pancrcatitis. Thus, 196 pts were evaluated for post ERCP pancmatitis. Post ERCP pancreatitis was defined as having abdominal pain necessitating narcotics, a two-fold elevation in amylase and an extra day stay in the hospital after ERCP. The number of PD injections and acinarization of the parenchyma were recorded. RESULTS: Nine out of 195 pts developed post ERCP pancreatitis (4.5%). Twelve pts had acinarization during ERCP, but none of these developed pancreatitis. The number of injections in all pts ranged from 1 to 8. Those developing pancreatitis had 3 or less PD injections. Of the 9 pts who developed pancreatitis, only 1 had diagnostic ERCP. The frequency of complex procedures were similar in the group who did not develop pancreatitis.
-
PD INJECTIONS (n) PANCREATITIS YES
1-3
4-8
9
0
ACINARIZATION 0
NO 131 56 12 CONCLUSION: T te number of PD injections and parenchymal acinarization does not correlate with post ERCP pancreatitis in this group. However. none of the pts in this study had greater than 8 PD injections. We suspect that post ERCP pancreatitis is multifactorial and unrelated to the number of PD injections and parenchymal acinarization.
552
550 CHRONIC PANCREATITIS (PCS) DUE TO ERCP-INDUCED PANCREATIC DUCT INJURY. Simon K Lo, Rabia K6ksal. Eric R Lee. Harbor-UCLA Medical Center and Torrance Memorial Medical Center. Torrance, California Acute PCS following ERCP is common, but long-term pancreatic complications due to ERCP is rarely reported. Aim: To characterize long-term pancreatic complications and management outcome. Method: Retrospective review of all pancreatic diseases that followed a ERCP at a referral center over a 6-year span. Cases of preexisting PCS, hyperamylasemia, abnormal pancreatography or frequent alcohol use were excluded. All patients (pts) underwent CT and a second ERCP to characterize their pancreaticobiliary anatomy. Pancreatic sphincter (PS) manometry or PS stenting trials were attempted in all pts since 1992. Results: Seven pts were identified, 6 had undergone their original ERCP elsewhere and 1 at our center. Indications were eholangitis (1) and probable eholedocholithiasis (CBDS) (6), Findings included CBDS (3), probable biliary sphincter stenosis (2), normal and failed cholangiogram (1 each). All 7 had normal pancreatograms. All except the normal and failed cholangiogram cases underwent a biliary sphincterotomy. Six pts developed PCS immediately post-ERCP (3 severe, 2 moderate and 1 mild), followed by persistent chronic PCS pain Median duration of symptoms prior to our evaluations was 36 months (3-120 months). Six pts ($6%) were found to have new major pancreatic PS stenosis based on difficult cannalations (6), obstructed PS on minor PS injections (2), hypertensive PS (2) and dramatic response to PS stenting (1). 3 pts had ductal strictures. Only 1 pt (14%), with a prior subtotal pancreatectomy, had a normal pancreatic duct and caunulatinn. Five pts were treated endoscopieally that included a PS sphincterotomy in all of them. The remaining 2 underwent surgical explorations, radiologic drainages and a permanent epidural anesthctic infusion. Of the 5 endoscopieally treated pts, 2 reported complete symptom resolution, 1 with dramatic and 2 mild but lasting improvement. Conclusions: 1) though rare, acute pancreatic injury due to diagnostic or therapeutic ERCP may progress to chronic PCS; 2) PS and/or ductal stenosis occurred in most of these pts, providing further evidence that the major mechanism of ERCP induced PCS is injury to the PS; 3) prognosis of isolated PS stenosis due to ERCP is good, as it responds to endoscopic pancreatic sphincterotomy; and 4) all patients with protracted pancreatic symptoms following ERCP should be evaluated with an ERCP and PS manometry.
AB162
Factors Possibly Influencing Post-ERCP Pancreatitis
GASTROINTESTINAL ENDOSCOPY
ENDOSCOPIC RESECTION OF HETEROTOPIC PANCREAS OF THE MINOR DUODENAL PAPILLA. J. E Lucena, O. A.. Alvarez, G. W.W. Gross. Dept. of Medicine UTHSC, San Antonio, Texas. Heterotopm pancreas (HP) is a focus of well developed, normally organized pancreatic tissue in anatomically aberrant location. HP has been detected in the duodenum, stomach, jejunum, ampulla of Vater, gallbladder, bile duct, and other sites. HP is subject to all the diseases of the pancreas proper, including malignant transformation. Benign submucosal tumors within the minor papilla are exceedingly rare and confusion with carcinoma may lead to extensive surgical resection. Endoscopic surgical techniques has expanded management options for submucosal lesions. We report our experience with the first documented case, to our knowledge, of HP in the minor papilla, as well as the first endoscopic resection of the minor papilia. A 73 y/o male with a history of epigastric pain and heartburn for several weeks, anemia and guaic positive stool was referred for endoscopy. He denied associated symptoms. PMH included DM, HTN, CAD, GERD, colon polyps, and no prior surgeries. PE revealed normal vital signs; abdomen was soft, nontender, and without mass. Significant labs included: hematocrit 30.5%, iron 57 mcg/dl. Abd sono was normal. EGD revealed a 1.8-xl.8-cm nodular mass with central umbilication in the second portion of the duodenum. Side-view duodenoscopy showed the lesion to be located in the minor duodenal papilla; the major papilla was normal. Biopsies were nondiagnostic. ERCP revealed dominant pancreatic drainage via the ventral duct and no effacement of the dorsal duct by tumor. EUS was unavailable. The tumor was removed with snare electroeautery. Dorsal duct stenting was not performed. Pathology revealed a nodule of normal pancreatic tissue, covered by normal duodenal mucosa, c/w HP of the minor papilla. F/U duodenoscopy after one year, detected no local tumor recun~nce and the patient remained asymptomatic. In summary, we described the first case of HP in the minor papilla with endoscopic resection. In the present em ERCP and EUS (where available) are essential tools in the diagnosis of major and minor papilla tumors. In a select group of high risk patients, endoscopic resection is an alternative treatment which may avoid the potential complication of open surgical resection.
VOLUME 45, NO. 4, 1997
551
ENDOSCOPIC TREATMENT OF PANCREATIC PSEUDOCYSTS. ED Libera JR, ES Siqueira, MRS Rohr, EP Maceclo, AP Ferrari, Endoscopy Unit, Division of Gastroenterology, UNIFESP - Escola Paulista de Medicina, S~o Pauio Brazil. Pancreatic pseudocysts have been successfully treated by endoscopic drainage (cystogastrostomy, cystoduodenostomy and transpapiltaw). We report our experience with endoscopic therapy of pancreatic pseudocysts. From July/94 to November/96, 27 patients with pancreatic pseudocysts ware referred to ERCP because of persistent pain and/or jaudice. In 6127 (22%) endoscopic therapy was not perfomed: pancreatic stenosis could not be crossed (3), there was no indentation of gastric or duodenal wall (2) and a B-II gastrectomy prevented access to the papilla (1). 21 patients, malelfemale ratio 18/3, mean age 36 years (range 24-64 years), 29 pseudocysts ware treated with cystogastrostomy (8), cystoduodenostomy (5) and transpapillary drainage (12). Etiology was: alcoholic chronic pancreatitis (17), blunt abdominal trauma (2) or surgical trauma (2). Pseudocysts mean size was 7,64 cm (range 3,5-20 cm) and they ware located in the head (10), body (14) and tail (5) of the pancreas. Complications were present in 8/27 patients: fever (1), asymptomatic pneumoperitoneum (1), bleeding (3), stent proximal migration (1), perforation (1) and pancraatitis (1). The patient with perforation required surgery, while all other complications ware minor and managed medically and/or endoscopically. There was no mortality. Mean follow up was 225 days (range 30-480 days) and mean stent period was 76 days for transpapillary stents, 41 days for cystogastrostomy and 40 days for cystoduodenostomy. Clinical improvement and pseudocysts resolution ocurred in 19/21 (90%): 15 are asymptomatic and 4 are taking small doses of analgesics. In 2 patients that persisted with pain, sugery was performed. We concluded that endoscopic therapy of pancreatic pseudocysts is a safe procedure, resulting in clinical improvement in most of the patients and recurrence is uncommon in the first year.
POST ERCP PANCREATITIS: DOES ACINARIZATION OR REPEATED PANCREATIC DUCT (PD) INJECTIONS INCREASE THE RISK - A PROSPECTIVE STUDY. NE Lobe, B Dahrnan, JE Geenen, WJ Hogan, MJ Schmalz, MF Catalano, GK Johnson, DJ Gecnen. St. Luke's Medical Center, Pancreatic Biliary Center, Milwaukee, Wisconsin. The most frequent complication of ERCP is pancreatitis occurring in 310% of pts. Potential risks associated with post ERCP pancreatitis are the number of PD injections and acinarization of the parenchyma. AIM: To determine whether the number of PD injections or parenchymal acinarization increases the risk of post ERCP pancreatitis. METHODS: We prospectively evaluated 330 consecutive pts undergoing both diagnostic and therapeutic ERCP (119 male, 211 female; average age 50.8 years). PD injections were not performed in 81 pts and these were excluded as were 53 pts with chronic pancrcatitis. Thus, 196 pts were evaluated for post ERCP pancmatitis. Post ERCP pancreatitis was defined as having abdominal pain necessitating narcotics, a two-fold elevation in amylase and an extra day stay in the hospital after ERCP. The number of PD injections and acinarization of the parenchyma were recorded. RESULTS: Nine out of 195 pts developed post ERCP pancreatitis (4.5%). Twelve pts had acinarization during ERCP, but none of these developed pancreatitis. The number of injections in all pts ranged from 1 to 8. Those developing pancreatitis had 3 or less PD injections. Of the 9 pts who developed pancreatitis, only 1 had diagnostic ERCP. The frequency of complex procedures were similar in the group who did not develop pancreatitis.
-
PD INJECTIONS (n) PANCREATITIS YES
1-3
4-8
9
0
ACINARIZATION 0
NO 131 56 12 CONCLUSION: T te number of PD injections and parenchymal acinarization does not correlate with post ERCP pancreatitis in this group. However. none of the pts in this study had greater than 8 PD injections. We suspect that post ERCP pancreatitis is multifactorial and unrelated to the number of PD injections and parenchymal acinarization.
552
550 CHRONIC PANCREATITIS (PCS) DUE TO ERCP-INDUCED PANCREATIC DUCT INJURY. Simon K Lo, Rabia K6ksal. Eric R Lee. Harbor-UCLA Medical Center and Torrance Memorial Medical Center. Torrance, California Acute PCS following ERCP is common, but long-term pancreatic complications due to ERCP is rarely reported. Aim: To characterize long-term pancreatic complications and management outcome. Method: Retrospective review of all pancreatic diseases that followed a ERCP at a referral center over a 6-year span. Cases of preexisting PCS, hyperamylasemia, abnormal pancreatography or frequent alcohol use were excluded. All patients (pts) underwent CT and a second ERCP to characterize their pancreaticobiliary anatomy. Pancreatic sphincter (PS) manometry or PS stenting trials were attempted in all pts since 1992. Results: Seven pts were identified, 6 had undergone their original ERCP elsewhere and 1 at our center. Indications were eholangitis (1) and probable eholedocholithiasis (CBDS) (6), Findings included CBDS (3), probable biliary sphincter stenosis (2), normal and failed cholangiogram (1 each). All 7 had normal pancreatograms. All except the normal and failed cholangiogram cases underwent a biliary sphincterotomy. Six pts developed PCS immediately post-ERCP (3 severe, 2 moderate and 1 mild), followed by persistent chronic PCS pain Median duration of symptoms prior to our evaluations was 36 months (3-120 months). Six pts ($6%) were found to have new major pancreatic PS stenosis based on difficult cannalations (6), obstructed PS on minor PS injections (2), hypertensive PS (2) and dramatic response to PS stenting (1). 3 pts had ductal strictures. Only 1 pt (14%), with a prior subtotal pancreatectomy, had a normal pancreatic duct and caunulatinn. Five pts were treated endoscopieally that included a PS sphincterotomy in all of them. The remaining 2 underwent surgical explorations, radiologic drainages and a permanent epidural anesthctic infusion. Of the 5 endoscopieally treated pts, 2 reported complete symptom resolution, 1 with dramatic and 2 mild but lasting improvement. Conclusions: 1) though rare, acute pancreatic injury due to diagnostic or therapeutic ERCP may progress to chronic PCS; 2) PS and/or ductal stenosis occurred in most of these pts, providing further evidence that the major mechanism of ERCP induced PCS is injury to the PS; 3) prognosis of isolated PS stenosis due to ERCP is good, as it responds to endoscopic pancreatic sphincterotomy; and 4) all patients with protracted pancreatic symptoms following ERCP should be evaluated with an ERCP and PS manometry.
AB162
Factors Possibly Influencing Post-ERCP Pancreatitis
GASTROINTESTINAL ENDOSCOPY
ENDOSCOPIC RESECTION OF HETEROTOPIC PANCREAS OF THE MINOR DUODENAL PAPILLA. J. E Lucena, O. A.. Alvarez, G. W.W. Gross. Dept. of Medicine UTHSC, San Antonio, Texas. Heterotopm pancreas (HP) is a focus of well developed, normally organized pancreatic tissue in anatomically aberrant location. HP has been detected in the duodenum, stomach, jejunum, ampulla of Vater, gallbladder, bile duct, and other sites. HP is subject to all the diseases of the pancreas proper, including malignant transformation. Benign submucosal tumors within the minor papilla are exceedingly rare and confusion with carcinoma may lead to extensive surgical resection. Endoscopic surgical techniques has expanded management options for submucosal lesions. We report our experience with the first documented case, to our knowledge, of HP in the minor papilla, as well as the first endoscopic resection of the minor papilia. A 73 y/o male with a history of epigastric pain and heartburn for several weeks, anemia and guaic positive stool was referred for endoscopy. He denied associated symptoms. PMH included DM, HTN, CAD, GERD, colon polyps, and no prior surgeries. PE revealed normal vital signs; abdomen was soft, nontender, and without mass. Significant labs included: hematocrit 30.5%, iron 57 mcg/dl. Abd sono was normal. EGD revealed a 1.8-xl.8-cm nodular mass with central umbilication in the second portion of the duodenum. Side-view duodenoscopy showed the lesion to be located in the minor duodenal papilla; the major papilla was normal. Biopsies were nondiagnostic. ERCP revealed dominant pancreatic drainage via the ventral duct and no effacement of the dorsal duct by tumor. EUS was unavailable. The tumor was removed with snare electroeautery. Dorsal duct stenting was not performed. Pathology revealed a nodule of normal pancreatic tissue, covered by normal duodenal mucosa, c/w HP of the minor papilla. F/U duodenoscopy after one year, detected no local tumor recun~nce and the patient remained asymptomatic. In summary, we described the first case of HP in the minor papilla with endoscopic resection. In the present em ERCP and EUS (where available) are essential tools in the diagnosis of major and minor papilla tumors. In a select group of high risk patients, endoscopic resection is an alternative treatment which may avoid the potential complication of open surgical resection.
VOLUME 45, NO. 4, 1997