Setting Of Chronic Pancreatitis Research Articles

Mechanisms of parenchymal injury and signaling pathways in ectatic ducts of chronic pancreatitis: implications for pancreatic carcinogenesis

The pathobiology of chronic pancreatitis (CP) remains enigmatic despite remarkable progress made recently in uncovering key mechanisms involved in the initiation and progression of the disease. CP is increasingly thought of as a multifactorial disorder. Apoptosis plays a role in parenchymal destruction, the pathological hallmark of CP. The apoptotic mechanisms preferentially target the exocrine compartment, leaving endocrine islets relatively intact for a prolonged period. Exocrine cells shed their ‘immunoprivileged' status, express death receptors, and are rendered susceptible to apoptosis induced by death ligands on infiltrating lymphocytes, and released locally by activated pancreatic stellate cells. Islet cells retain their ‘immunoprivileged' status and activate anti-apoptotic programs through NF-κB. Ductal changes, including distortion, dilatation, and pancreatic ductal hypertension in the setting of CP, induce genomic damage and increased cell turnover. In addition, signaling mechanisms that play a role in the development of embryonic pancreas are reinstated, thus, playing a role in repair, regeneration, and transformation. This, in turn, leads to acino-ductal metaplasia (ADM) and pancreatic intraepithelial neoplasia (PanIN). Some of these pathways are activated in pancreatic cancer. We attempt to integrate the current knowledge and major concepts in the pathogenesis of CP and to explain the mechanism of differential cell loss. We also discuss the possible implications of signaling pathway activation in pancreatic inflammation, relevant to the cellular transformation that leads to pancreatic neoplasia.

Direct percutaneous puncture embolization of a peripancreatic pseudoaneurysm presenting with haemosuccus pancreaticus

Haemosuccus pancreaticus is a rare cause of gastrointestinal haemorrhage. It is commonly due to a pseudoaneurysm in a setting of chronic pancreatitis. Treatment of aneurysms has traditionally been surgery; however, recently percutaneous radiological intervention has achieved good results with minimum morbidity and mortality. Transcatheter embolization of aneurysms is an effective treatment option. However, not all aneurysms are accessible through this route. We describe a technique of direct puncture embolization of a pseudoaneurysm causing haemosuccus pancreaticus.

Pancreatic pseudocyst in the setting of chronic pancreatitis and pancreas divisum

Pancreatic pseudocyst in the setting of chronic pancreatitis and pancreas divisum

Endoscopic therapy for chronic pancreatitis: An evidence-based review

In the setting of chronic pancreatitis, pancreatic ductal obstruction, and ductal leak, pseudocyst formation and biliary obstruction present many challenges for endoscopists. Although chronic pancreatitis has a variety of clinical manifestations, most commonly patients present with intermittent or chronic abdominal pain. Recent studies suggest stenting of pancreatic ductal strictures has a significant impact on reducing chronic pain. The removal of ductal calculi, presumably from relieving obstruction, also improves abdominal pain. When the site of leak is bypassed, ductal leaks may be cured by endoscopic stenting. Multiple plastic bile duct stents to treat chronic pancreatitis-associated bile duct stricture can delay the need for surgery. Although these endoscopic techniques have been beneficial for many patients, further study is warranted to better define their role in chronic pancreatitis compared with well-established surgical techniques.

Diffusion-Weighted MR Imaging in the Evaluation of Pancreatic Exocrine Function Before and After Secretin Stimulation

To evaluate diffusion weighted MR imaging before and after secretin stimulation in the assessment of pancreatic exocrine function in the setting of chronic pancreatitis. Nine patients with severe chronic pancreatitis and sixteen patients without chronic pancreatitis but with a history of chronic alcohol consumption were enrolled in the chronic pancreatitis and risk groups, respectively. Thirty-eight patients without any pancreatic disease or history of alcohol consumption were included in the control group. Diffusion weighted images were obtained before and after secretin administration in all patients. The peak ADC values and times were determined and intergroup differences were compared. A receiver operating characteristic curve (ROC) was used to identify the cutoff values of the peak ADC times for discrimination of control group from risk and chronic pancreatitis groups. In the control group, a peak increase in ADC value of 57-120% (median: 75%) was observed between 90 s and 4 min (median: 2 min) after administration of secretin (Pattern 1). In the risk group, in 13 patients, a peak increase of 52-150% was observed between 4 and 8 min (median: 7 min; Pattern 2). Peak times were significantly longer in risk group (p < 0.01). In three patients in the risk group, and in all patients in the chronic pancreatitis group, no ADC peak was observed within 10 min following secretin administration (Pattern 3). Using a peak time of 4 min as the cut-off value, a sensitivity of 100% and specificity of 94.7% were achieved in discriminating the control group from the combined risk and chronic pancreatitis groups. Diffusion-weighted MR imaging before and after secretin administration could yield clinically useful information for detecting pathophysiologic alterations in the setting of chronic pancreatitis.

Yield of EUS-guided FNA of pancreatic masses in the presence or the absence of chronic pancreatitis

Evaluation of a focal pancreatic mass in the setting of chronic pancreatitis (CP) is a diagnostic challenge. The objectives of the study were to compare the diagnostic yield and accuracy of EUS-guided FNA (EUS-FNA) in the evaluation of pancreatic-mass lesions in the presence or the absence of CP and to identify predictors of CP before EUS-FNA of pancreatic-mass lesions. The study design was analysis of data collected prospectively on all patients with solid pancreatic-mass lesions who underwent EUS-FNA at a tertiary referral center. A total of 282 consecutive patients underwent 300 EUS-FNA procedures of pancreatic-mass lesions over a 3-year period. The diagnostic yield and the accuracy of EUS-FNA was compared between patients with and without CP. CP was defined by the presence of more than 4 EUS criteria. Final diagnosis was adenocarcinoma in 210 (70%), benign disease in 64 (21%), other pathology in 19 (6%), and indeterminate in 4 (2%); 3 patients (1%) were lost to follow-up. CP was noted in 75/300 (25%) patients. A lower sensitivity for EUS-FNA was observed in patients with CP than in those without CP (73.9% vs. 91.3%; p = 0.02). While patients with CP had a higher negative predictive value (88.9% vs. 45.5%; p < 0.001), no significant differences were observed for specificity (100% vs. 93.8%), positive predictive value (100% vs. 99.5%), and accuracy (91.5% vs. 91.4%) between those with and without CP. False-negative cytology was encountered in 24 cases: 6/71 (8%) with CP vs. 18/222 (8%) without CP. Patients with CP required more EUS-FNA passes to establish a diagnosis vs. those without CP (median, 5 vs. 2; p < 0.001). On multivariable analysis, age < 50 years (p < 0.001), male gender (p < 0.001), black race (p = 0.001), and the absence of jaundice (p = 0.005) were significantly associated with CP. The impact of EUS-FNA on long-term clinical management was not analyzed. The impact of individual EUS features of CP on sensitivity of EUS-FNA was not evaluated. By protocol, mass lesions that were benign required more passes to definitively exclude malignancy. EUS-FNA has a low sensitivity for pancreatic-mass lesions in the setting of CP. This decreased sensitivity can be overcome by performing more numbers of passes at FNA, which improves diagnostic accuracy. Demographic features and clinical presentation are predictive of underlying CP in patients with pancreatic-mass lesions.

Temporary Spontaneous Thrombosis of a Splenic Artery Pseudoaneurysm in Chronic Pancreatitis during Intravenous Octreotide Administration

Splenic artery pseudoaneurysm is a well-known and potentially life-threatening complication of pancreatitis for which immediate endovascular or surgical treatment is indicated. An unusual case of spontaneous thrombosis of a splenic artery pseudoaneurysm with associated partial splenic infarction was encountered in the setting of chronic pancreatitis during intravenous octreotide administration, with recanalization 9 months later.

Gene expression alterations in the non-neoplastic parenchyma adjacent to infiltrating pancreatic ductal adenocarcinoma

The non-neoplastic pancreatic parenchyma adjacent to infiltrating ductal adenocarcinoma demonstrates inflammation, fibrosis, acinar cell loss and small duct-like metaplasia of acinar cells. Similar morphologic changes are also observed in the setting of chronic pancreatitis. In addition, peritumoral acini have been shown to have alterations in gene expression even in the absence of morphological changes. To better understand the pancreatic acinar responses to infiltrating pancreatic ductal adenocarcinoma, we characterized gene expression patterns of pancreatic acinar tissue adjacent to infiltrating pancreatic ductal adenocarcinomas and compared them to gene expression patterns of acinar tissue affected by chronic pancreatitis as well as to those of normal pancreatic acini. Fresh-frozen pancreatic acinar tissue was microdissected from nine patients (three with pancreatic cancer, three with chronic pancreatitis, three with normal pancreata) using laser capture microdissection, and extracted RNA from each microdissection was subjected to two rounds of linear amplification and hybridized to oligonucleotide microarrays. Gene expression patterns were confirmed using quantitative RT-PCR and/or immunohistochemistry. A total of 20 genes was found to be overexpressed in peritumoral acinar tissue compared to normal acinar tissue and to acini affected by chronic pancreatitis. These 20 genes included pancreatitis-associated protein (HIP/PAP), a gene known to be overexpressed in acini adjacent to infiltrating pancreatic cancer, and the gene cartilage glycoprotein-39 (HC gp-39 or TKL-40). Serum HC gp-39 protein levels were significantly higher in patients with pancreatic cancer and in those with chronic pancreatitis than in controls without pancreatic disease. There was no significant difference in the levels of serum HC gp-39 in patients with pancreatic cancer and those with chronic pancreatitis. Our results demonstrate some of the molecular alterations in acinar cells that occur in response to adjacent infiltrating pancreatic ductal adenocarcinoma and reveal that such alterations can provide a rich source of markers of pancreatic cancer.

Yield of EUS-FNA of Pancreatic Masses in the Presence or Absence of Chronic Pancreatitis

Background: Evaluation of a focal pancreatic mass in the setting of chronic pancreatitis (CP) is a diagnostic challenge. The few studies conducted in this context are from Europe and the results are disappointing. Aim: 1) To compare the diagnostic yield and accuracy of EUS-FNA in the evaluation of pancreatic mass lesions in the presence or absence of CP in a North American population and 2) Identify predictors of CP prior to EUS-FNA of pancreatic mass lesions. Methods: Prospective study of 300 consecutive patients who underwent EUS-FNA of pancreatic mass lesions over a three year period. Chronic pancreatitis was defined by the presence of > 4 EUS criteria. The diagnostic yield and accuracy of EUS-FNA was compared between patients with and without CP. Multivariable logistic regression was used to identify predictors for CP. Results: Final diagnosis was adenocarcinoma in 210 (70%), benign disease in 64 (21%), other pathology in 19 (6%), and indeterminate in 4 (2%); 3 patients (1%) were lost to follow-up. CP was noted in 75/300 (25%) patients. A lower sensitivity for EUS-FNA was observed in patients with CP than those without CP (73.9% vs. 91.3%; p=0.02). While patients with CP had a higher NPV (88.9% vs. 45.5%; p<0.001), no significant differences were observed for specificity (100% vs. 93.8%), PPV (100% vs. 99.5%) and accuracy (91.5% vs. 91.4%) between those with and without CP. False negative cytology was encountered in 24 cases: 6/71 (8%) with CP versus 18/222 (8%) without CP. Patients with CP required more EUS-FNA passes to establish diagnosis versus those without CP (median, 5 versus 2; p < 0.001). On multivariable analysis, age < 50 (p <0.001), male sex (p < 0.001), black race (p = 0.001), and absence of jaundice at clinical presentation (p = 0.005) were significantly associated with CP. Conclusions: EUS-FNA has a low sensitivity for pancreatic mass lesions in the setting of chronic pancreatitis. This decreased sensitivity can be overcome by performing more number of passes at FNA which improves diagnostic accuracy. Demographic features and clinical presentation are predictive of underlying chronic pancreatitis in patients with pancreatic mass lesions. Background: Evaluation of a focal pancreatic mass in the setting of chronic pancreatitis (CP) is a diagnostic challenge. The few studies conducted in this context are from Europe and the results are disappointing. Aim: 1) To compare the diagnostic yield and accuracy of EUS-FNA in the evaluation of pancreatic mass lesions in the presence or absence of CP in a North American population and 2) Identify predictors of CP prior to EUS-FNA of pancreatic mass lesions. Methods: Prospective study of 300 consecutive patients who underwent EUS-FNA of pancreatic mass lesions over a three year period. Chronic pancreatitis was defined by the presence of > 4 EUS criteria. The diagnostic yield and accuracy of EUS-FNA was compared between patients with and without CP. Multivariable logistic regression was used to identify predictors for CP. Results: Final diagnosis was adenocarcinoma in 210 (70%), benign disease in 64 (21%), other pathology in 19 (6%), and indeterminate in 4 (2%); 3 patients (1%) were lost to follow-up. CP was noted in 75/300 (25%) patients. A lower sensitivity for EUS-FNA was observed in patients with CP than those without CP (73.9% vs. 91.3%; p=0.02). While patients with CP had a higher NPV (88.9% vs. 45.5%; p<0.001), no significant differences were observed for specificity (100% vs. 93.8%), PPV (100% vs. 99.5%) and accuracy (91.5% vs. 91.4%) between those with and without CP. False negative cytology was encountered in 24 cases: 6/71 (8%) with CP versus 18/222 (8%) without CP. Patients with CP required more EUS-FNA passes to establish diagnosis versus those without CP (median, 5 versus 2; p < 0.001). On multivariable analysis, age < 50 (p <0.001), male sex (p < 0.001), black race (p = 0.001), and absence of jaundice at clinical presentation (p = 0.005) were significantly associated with CP. Conclusions: EUS-FNA has a low sensitivity for pancreatic mass lesions in the setting of chronic pancreatitis. This decreased sensitivity can be overcome by performing more number of passes at FNA which improves diagnostic accuracy. Demographic features and clinical presentation are predictive of underlying chronic pancreatitis in patients with pancreatic mass lesions.

Accuracy of Magnetic Resonance Cholangiopancreatography (MRCP) in the Diagnosis of Pancreas Divisum (PD)

Background: Patients with PD may develop recurrent acute or chronic pancreatitis. ERCP is the gold standard for diagnosing PD. MRCP is a non invasive test reported to be highly accurate in diagnosing PD (Matos et al. GI Endosc 2001;53:728-33, Bret et al. Radiol 1996; 199:99-103). Aim: To evaluate the diagnostic accuracy of MRCP in detecting PD at our institution. Methods: During a 22-month period (10/02-07/04), 205 patients underwent ERCP and MRCP for various indications. 146 patients had diagnostic endoscopic pancreatograms (ERP) after MRCP and comprise our study population. MRCP was performed with the 1.5 T Signa Horizon LX scanner (GE Imaging Systems, Milwaukee, WI). Secretin 16 mg (SecreFlo™, ChiRhoClin, Burtonsville, MD) was given in 113/146 patients (S-MRCP). The remaining 33/146 had MRCP without secretin. Since 7/33 MRCP without secretin (21.2%) were non-diagnostic, further study focused on S-MRCP only. The S-MRCP was interpreted prior to ERP by 4 gastrointestinal radiologists as part of the routine daily workload and compared to subsequent ERP results. Results: 113 patients with S-MRCP and ERP (54 male, mean age 47.1 years) were evaluated. ERP identified PD in 19/113 (16.8%). S-MRCP identified 14/19 PD and was false positive in 3 cases (sensitivity 73.3%, specificity 96.8%, positive predictive value 82.4%, negative predictive value 94.8%). Five of 8 patients (63%) with inaccurate S-MRCP had changes of chronic pancreatitis by ERP. This differs from the frequency of chronic pancreatitis by ERP in 24/105 patients (25%) with accurate MRCP findings (p = 0.03). Summary: S-MRCP had a satisfactory specificity for detecting PD. However, the sensitivity of S-MRCP for diagnosis of PD was modest at 73.3%. This is low compared to previous smaller studies, which reported a sensitivity of MRCP up to 100%. Conclusions: 1) Our experience at a large referral center does not reflect the high diagnostic accuracy of MRCP for PD in previous studies. 2) MRCP without secretin results in a high percentage of non-diagnostic studies and should be obsolete if pancreatic assessment is desired. 3) It is more difficult to diagnose PD by MRCP in the setting of chronic pancreatitis. Background: Patients with PD may develop recurrent acute or chronic pancreatitis. ERCP is the gold standard for diagnosing PD. MRCP is a non invasive test reported to be highly accurate in diagnosing PD (Matos et al. GI Endosc 2001;53:728-33, Bret et al. Radiol 1996; 199:99-103). Aim: To evaluate the diagnostic accuracy of MRCP in detecting PD at our institution. Methods: During a 22-month period (10/02-07/04), 205 patients underwent ERCP and MRCP for various indications. 146 patients had diagnostic endoscopic pancreatograms (ERP) after MRCP and comprise our study population. MRCP was performed with the 1.5 T Signa Horizon LX scanner (GE Imaging Systems, Milwaukee, WI). Secretin 16 mg (SecreFlo™, ChiRhoClin, Burtonsville, MD) was given in 113/146 patients (S-MRCP). The remaining 33/146 had MRCP without secretin. Since 7/33 MRCP without secretin (21.2%) were non-diagnostic, further study focused on S-MRCP only. The S-MRCP was interpreted prior to ERP by 4 gastrointestinal radiologists as part of the routine daily workload and compared to subsequent ERP results. Results: 113 patients with S-MRCP and ERP (54 male, mean age 47.1 years) were evaluated. ERP identified PD in 19/113 (16.8%). S-MRCP identified 14/19 PD and was false positive in 3 cases (sensitivity 73.3%, specificity 96.8%, positive predictive value 82.4%, negative predictive value 94.8%). Five of 8 patients (63%) with inaccurate S-MRCP had changes of chronic pancreatitis by ERP. This differs from the frequency of chronic pancreatitis by ERP in 24/105 patients (25%) with accurate MRCP findings (p = 0.03). Summary: S-MRCP had a satisfactory specificity for detecting PD. However, the sensitivity of S-MRCP for diagnosis of PD was modest at 73.3%. This is low compared to previous smaller studies, which reported a sensitivity of MRCP up to 100%. Conclusions: 1) Our experience at a large referral center does not reflect the high diagnostic accuracy of MRCP for PD in previous studies. 2) MRCP without secretin results in a high percentage of non-diagnostic studies and should be obsolete if pancreatic assessment is desired. 3) It is more difficult to diagnose PD by MRCP in the setting of chronic pancreatitis. ErratumGastrointestinal EndoscopyVol. 62Issue 2PreviewIn the DDW 2005 Abstract issue (Volume 61, Number 5), two abstracts contained a typographical error in one author's name. For the abstracts “Accuracy of Magnetic Resonance Cholangiopancreatography (MRCP) in the Diagnosis of Pancreas Divisum (PD)” (Gastrointest Endosc 2005:61:AB100) and “ERCP Findings in Idiopathic Pancreatitis (IP): Cystic Fibrosis (CF) Gene Positive and Negative Patients” (Gastrointest Endosc 2005;61:AB186), the correct spelling of the author's name is Waleed Alazmi. Full-Text PDF

Tissue glue for the endoscopist: Healing by sealing

Tissue glue for the endoscopist: Healing by sealing

FDG-PET is able to detect pancreatic carcinoma in chronic pancreatitis

2-(18F)-fluoro-2-deoxy-D-glucose positron emission tomography (FDG-PET) is an imaging technique which enables detection of malignancies. FDG-PET has been established as a tool for the diagnosis of pancreatic carcinoma (CA). Early detection is mandatory as cure can only be achieved in non-advanced disease. This is, however, very difficult with conventional radiological techniques. Patients with chronic pancreatitis (CP) are at risk of developing CA. A simple, reliable screening method for malignant degeneration is highly desirable. We set out to investigate whether FDG-PET is able to detect CA in the setting of CP and can fulfil a potential role in the early detection of CA in CP. FDG-PET was performed in 77 CP patients and in six patients with CP complicated by CA (CP + CA). We included 26 CA patients as a positive control. A positive scan was defined as focal FDG accumulation in the pancreas region. In 67 of the 77 CP (87%) patients, pancreatic FDG accumulation was absent. Six patients had significant accumulation. In CA, 24/26 patients had a positive PET. Five out of the six patients with CP + CA had focal uptake, while minor uptake was seen in one patient. FDG-PET was positive in almost all CA patients and CP + CA patients. FDG-PET was negative in the large majority (87%) of CP patients, which suggests that a positive PET scan in CP patients must lead to efforts to exclude a malignancy. These data suggest that FDG-PET has a potential role as a diagnostic tool for detecting CA in longstanding CP.

The Ascites to Serum Amylase Ratio Identifies Two Distinct Populations in Acute Pancreatitis with Ascites

Background/Aim: While the characteristics of ascites in the setting of chronic pancreatitis are well established, little has been written about the characteristics of spontaneous, clinically apparent ascites in the setting of acute pancreatitis. Our aim was to define the characteristics of clinically apparent ascites complicating acute pancreatitis, particularly with regard to outcomes. Methods: We performed a search of our hospital’s discharge records for ICD codes 577.0 (acute pancreatitis) and 789.5 (ascites). Clinical and laboratory variables in survivors and nonsurvivors were compared using a Mann-Whitney U test. Results: We identified 59 records of which 25 cases had ascites fluid analysis. Only the ascites amylase (p = 0.033) and the ascites to serum amylase ratio (p = 0.002) correlated with mortality. Setting a cutoff of 1, the ascites to serum amylase ratio achieved a sensitivity of 83% and a specificity of 92% as a predictor of mortality. Conclusions: The ascites to serum amylase ratio identifies 2 sets of patients with ascites complicating acute pancreatitis. In patients with a high ratio, ascites may result from a localized duct disruption. In patients with a low ratio, ascites may be secondary to comorbid conditions or a capillary leak. In acute pancreatitis with clinically apparent ascites, the ascites to serum amylase ratio may be a predictor of mortality.

Optimising outcomes in acute pancreatitis.

Acute pancreatitis is a common cause for presentation to emergency departments. Common causes in Western societies include biliary pancreatitis and alcohol (the latter in the setting of chronic pancreatitis). Acute pancreatitis also follows endoscopic retrograde pancreatography in 5 to 10% of patients, a group that could potentially benefit from prophylactic treatment. Although episodes of pancreatitis usually run a relatively benign course, up to 20% of patients have more severe disease, and this group has significant morbidity and mortality. Therefore, attempts have been made to identify, at or soon after presentation, those patients likely to have a poor outcome and to channel resources to this group. The mainstay of treatment is aggressive support and monitoring of those patients likely to have a poor outcome. Pharmacotherapy for acute pancreatitis (both prophylactic and in the acute setting) has been generally disappointing. Efforts initially focused on protease inhibitors, of which gabexate shows some promise as a prophylactic agent. Agents that suppress pancreatic secretion have produced disappointing results in human studies. Infection of pancreatic necrosis is associated with high mortality and requires surgical intervention. In view of the seriousness of infected necrosis, the use of prophylactic antibacterials such as carbapenems and quinolones has been advocated in the setting of pancreatic necrosis. Similarly, data are accumulating to support the use of prophylactic antifungal therapy. Recently, it has become apparent that the intense inflammatory response associated with acute pancreatitis is responsible for much of the local and systemic damage. With this realisation, future efforts in pharmacotherapy are likely to focus on suppression or antagonism of pro-inflammatory cytokines and other inflammatory mediators. Similarly, animal studies have demonstrated the importance of oxidative stress in acute pancreatitis, although to date there is a paucity of information regarding the efficacy of antioxidants. Although the clinical course for most patients with acute pancreatitis is mild, severe acute pancreatitis continues to be a clinical challenge, requiring a multidisciplinary approach of physician, intensivist and surgeon.

Operative treatment of pseudocysts in patients with chronic pancreatitis.

Pseudocysts associated with chronic pancreatitis are generally intrapancreatic and associated with parenchymal disease. They tend to persist and cause complications. Minimally invasive methods of treatment challenge the traditional techniques of operative management. Surgical operation allows definitive treatment of the pseudocyst with the option of dealing appropriately with the diseased pancreas and excluding a neoplastic process. The aim of this study was to review the safety and efficacy of a surgical approach to the management of pseudocysts associated with chronic pancreatitis. A personal series of 112 consecutive patients operated for pseudocysts in the setting of chronic pancreatitis was reviewed. Chronic pancreatitis was confirmed by imaging studies in association with exocrine and/or endocrine failure. Cysts were multiple in 31 patients and presented with complications other than pain in 47. Data were collected prospectively regarding the clinical presentation, the nature of the operation and its outcome. Forty-eight patients (43 per cent) underwent drainage procedures, 56 (50 per cent) had a resection and eight (7 per cent) had a combination. Larger cysts and those located in the head and neck tended to be drained, while smaller and distal cysts were more often resected. The morbidity rate was 28 per cent and the operative mortality rate was 1 per cent. The cyst recurrence rate was 3 per cent and pain was relieved in 74 per cent of patients. Operative management of pseudocysts associated with chronic pancreatitis is effective with low morbidity and mortality rates. The introduction of newer minimally invasive techniques will have to withstand comparison to this traditional approach.

Pancreaticopleural fistula in chronic pancreatitis: resolution with endoscopic therapy

Pleural effusion most commonly has a cardiac or pulmonary etiology. Gastrointestinal/intra-abdominal causes include hepatic failure associated with ascites, malignancy, ruptured ectopic pregnancy, esophageal rupture, and pancreatitis. Sympathetic pleural effusion can complicate acute pancreatitis,1,2 and large pleural effusions may arise in the setting of chronic pancreatitis. Pancreatic ductal disruption can lead to fistulous tracts that extend along the esophageal and aortic hiati into the mediastinum.3 Additionally, direct penetration of fistulous tracts or intra-abdominal pseudocysts through the dome of the diaphragm into the pleural cavity are described.4-6 This is a case of pancreaticopleural fistula that presented with a massive pleural effusion as a manifestation of pancreatitis and a report of the successful treatment with nasopancreatic drainage.

4692 Recalcitrant pancreatic duct stones: successful removal following mechanical lithotripsy.

Pancreatic duct stones are usually a consequence of chronic pancreatitis. The presence of PD stones can result in acute exacerbation of pancreatitis or chronic abdominal pain. Successful removal of PD stones has been achieved in over 70% of patients from both ducts of Wirsung (ventral) and Santorini (dorsal). Limitations include adherent or large stones and the relative small size of pancreatic sphincterotomies. AIM: To determine the feasibility and effectiveness of mechanical lithotripsy of pancreatic duct stones. METHODS: Ninety-five patients with PD stones, including 28 patients with pancreas divisum in the setting of chronic pancreatitis over a 15 year period were identified using a computer data base retrieval system. Forty-two patients presented with acute pancreatitis while 53 patients presented with exacerbation of their abdominal pain. Of these, 13 patients required mechanical lithotripsy and are the subject of this report. Nine of 13 patients had single stones (8-12 mm) while 3 of 13 patients had multiple stones (6-10 mm). Ducts were dilated in all patients (6-16 mm). RESULTS: Successful stone extraction required 1-3 (mean 1.8 sessions). Endoscopic sphincterotomy was performed in all patients. Single stones were extracted in 8 of 9 patients (89%), multiple stones in 3 of 4 patients (75%). PD stents were placed after initial attempts at extraction (=5)and palliation (=2). Of the 2 patients with unsuccessful stone extraction, 1 underwent pancreaticojejunostomy with good long-term results. Of the 2 patients with failed stone extraction, both were treated intermittently with stents with recurrent symptoms (mean follow-up 3.8 years). Nine of 11 patients had complete stone extraction with 8 of these patients with good long-term (no pain/pancreatitis) results and no recurrence (mean follow-up 4.2 years). CONCLUSION: Endoscopic removal of recalcitrant PD stones can be accomplished in the majority of pts by mechanical lithotripsy with good long-term outcome. Those failing endoscopic therapy will often respond to surgical options. Pancreatic duct stones are usually a consequence of chronic pancreatitis. The presence of PD stones can result in acute exacerbation of pancreatitis or chronic abdominal pain. Successful removal of PD stones has been achieved in over 70% of patients from both ducts of Wirsung (ventral) and Santorini (dorsal). Limitations include adherent or large stones and the relative small size of pancreatic sphincterotomies. AIM: To determine the feasibility and effectiveness of mechanical lithotripsy of pancreatic duct stones. METHODS: Ninety-five patients with PD stones, including 28 patients with pancreas divisum in the setting of chronic pancreatitis over a 15 year period were identified using a computer data base retrieval system. Forty-two patients presented with acute pancreatitis while 53 patients presented with exacerbation of their abdominal pain. Of these, 13 patients required mechanical lithotripsy and are the subject of this report. Nine of 13 patients had single stones (8-12 mm) while 3 of 13 patients had multiple stones (6-10 mm). Ducts were dilated in all patients (6-16 mm). RESULTS: Successful stone extraction required 1-3 (mean 1.8 sessions). Endoscopic sphincterotomy was performed in all patients. Single stones were extracted in 8 of 9 patients (89%), multiple stones in 3 of 4 patients (75%). PD stents were placed after initial attempts at extraction (=5)and palliation (=2). Of the 2 patients with unsuccessful stone extraction, 1 underwent pancreaticojejunostomy with good long-term results. Of the 2 patients with failed stone extraction, both were treated intermittently with stents with recurrent symptoms (mean follow-up 3.8 years). Nine of 11 patients had complete stone extraction with 8 of these patients with good long-term (no pain/pancreatitis) results and no recurrence (mean follow-up 4.2 years). CONCLUSION: Endoscopic removal of recalcitrant PD stones can be accomplished in the majority of pts by mechanical lithotripsy with good long-term outcome. Those failing endoscopic therapy will often respond to surgical options.

Endoscopic retrograde cholangiopancreatography in the diagnosis and management of pancreatic diseases

Endoscopic retrograde cholangiopancreatography (ERCP) has been used for diagnosis and treatment of pancreatic diseases for over 20 years. ERCP has been most intensely investigated for acute biliary pancreatitis. Randomized trials have proven that its use will decrease morbidity and have suggested a decrease in mortality for patients with severe gallstone pancreatitis. ERCP is also valuable in detecting and treating main pancreatic duct leaks with transpapillary stenting. Symptomatic pseudocysts, which may be seen in either acute or chronic pancreatitis, can be drained via the papilla or through creation of a cystogastrostomy or cystoduodenostomy with a needle-knife sphincterotome. Endoscopic treatment of patients with recurrent acute pancreatitis presumed due to pancreas divisum and sphincter of Oddi dysfunction remains controversial. Dominant pancreatic strictures or calculi in the setting of chronic pancreatitis may be treated with stenting and removal of calculi to improve abdominal pain. Finally, diagnosis of pancreatic cancer by brush cytology and palliative management of biliary obstruction with various plastic and expandable metal sents have simplified management of this difficult problem.

Pancreatic-pleural fistula: the role of ERCP in diagnosis and treatment

Pleural effusion can develop in the setting of acute pancreatitis. The incidence varies from 3% to 17%, and up to 50% if CT is used for screening.1,2 The effusions are most commonly small, left-sided and thought to be lymphatic or sympathetic in origin. Pancreatic-pleural fistula, however, results from pancreatic duct disruption or pancreatic pseudocyst extension into the pleural cavity. This is an uncommon entity. It usually presents as a large, recurrent pleural effusion in the setting of chronic pancreatitis.

Endoscopic treatment of pancreatic duct strictures

Pancreatic duct strictures present one of the most challenging diagnostic and therapeutic pancreatic disorders. Patients present with a variety of symptoms, including recurrent or persistent abdominal pain, particularly in the setting of chronic pancreatitis. Other presenting symptoms may be those generally present in other patients with chronic pancreatitis and include weight loss, steatorrhea, nausea, and vomiting. The finding of pancreatic duct strictures often possess a diagnostic dilemna regarding a cause. Differential diagnosis includes acute and chronic pancreatitis, pseudocysts, and neoplasm. An accurate diagnosis requires one or more radiographic studies. Appropriate use of endoscopic retrograde cholangiopancreatography (ERCP) allows for the conformation of pancreatic duct strictures, diagnostic tissue sampling, and therapeutic treatment options. Endoscopic techniques in the treatment of strictures have included dilation and pancreatic duct stenting at variable intervals. Several studies have demonstrated the success of placement, safety, and efficacy of transpapillary stenting in benign disease, although follow-up data have been short. Complications of stenting have been reported to include stent migration, stent occlusion, episode of acute pancreatitis, and anatomic changes of the main pancreatic duct similar to chronic pancreatitis. Randomized, controlled clinical trials comparing the efficacy of endoscopic versus surgical treatment options are needed to establish the optimal, long-term therapy of benign pancreatic duct strictures.