Catalytic activity of phospholipase A<Subscript>2</Subscript> in blood plasma and pancreatic tissue perfusion in early experimental acute pancreatitis

BACKGROUND: To investigate the sequence of changes in the catalytic activity of phospholipase A2 in plasma and pancreatic tissue perfusion and oxygenation in mild and severe acute pancreatitis in pigs. METHODS: Twenty-four pigs were randomized into the groups of severe acute pancreatitis, mild acute pancreatitis, and controls. The pancreatic duct of eight anesthetized and mechanically ventilated pigs was cannulated, and taurocholic acid was infused into the pancreatic duct to induce severe acute pancreatitis. Eight animals received intraductal saline and developed mild acute pancreatitis. Eight pigs were cannulated only and served as controls. RESULTS: Central hemodynamics, arterial blood gases, and acid-base balance were stable throughout the study period in all three groups. Pancreatic tissue oxygenation decreased in pigs with severe acute pancreatitis and increased in animals with mild acute pancreatitis. The catalytic activity of phospholipase A2 in plasma remained stable, and there was no difference between the groups. Similarly, C-reactive protein values remained within the normal range during the study period in all groups. CONCLUSION: Plasma phospholipase A2 levels do not react to the changes in pancreatic tissue perfusion in the early phase of mild and severe acute pancreatitis.     

Central haemodynamics in experimental acute pancreatitis.

OBJECTIVE: To investigate central haemodynamics in severe and mild acute pancreatitis in pigs. DESIGN: Randomised controlled experiment. SETTING: Animal laboratory, Finland. SUBJECTS: 24 domestic pigs weighing 21-27 kg. INTERVENTIONS: In 8 anaesthetised and mechanically ventilated pigs the pancreatic duct was cannulated and taurocholic acid was infused to induce severe acute pancreatitis. Eight animals received intraductal saline infusion and developed mild acute pancreatitis. Eight pigs were cannulated alone and served as controls. MAIN OUTCOME MEASURES: Cardiac index, heart rate, mean arterial pressure, central venous pressure, mean pulmonary arterial pressure, pulmonary arterial occlusion pressure, haemoglobin, arterial blood gases and acid base balance. RESULTS: Intraductally infused taurocholic acid rapidly induced severe necrotising acute pancreatitis as assessed both macroscopically and histologically. Histological changes of mild acute pancreatitis were seen in animals after intraductal saline infusion. Central haemodynamics, arterial blood gases, and acid base balances were stable throughout the study period in all groups. The main finding was haemoconcentration as indicated by the increase in arterial haemoglobin concentration in pigs with mild and severe acute pancreatitis. CONCLUSION: Haemoconcentration precedes central haemodynamic alterations in experimental acute pancreatitis.     

大承气汤对急性重型胰腺炎大鼠血中可溶性粘附分子CD11a/CD1 8表达的影响

目的：进一步认识大承气汤对急性胰腺炎的治疗机理。方法：采用胰管内逆行注入牛磺胆酸钠方法造成大鼠急性重型胰腺炎模型,造模后用大承气汤、生理盐水进行治疗,观察造模治疗后12h、14h动物血清中CD11a/CD18、淀粉酶及胰腺组织中TNF含量的变化和胰腺组织病理学的改变。结果：应用大承气汤治疗组的大鼠血中的可溶性CD11a/CD18表达胰腺组织中的TNF含量、胰腺组织病理损害程度、胰酶血症的水平均较生理盐水治疗组明显下降或减轻。结论：认为大承气汤治疗急性重型胰腺炎的机理可能不仅在于其能促进胰酶的排出,还与其减少粘附分子CD11a/CD18的表达,减少胰腺组织中PMNs的浸润程度,进而减轻了胰腺组织损伤有关。     

Enterokinase induces severe necrosis and rapid mortality in cerulein pancreatitis: characterization of a novel noninvasive rat model of necro-hemorrhagic pancreatitis

BACKGROUND: Unlike edematous pancreatitis, induction of severe necrotizing pancreatitis in rats generally requires an invasive laparotomy with infusion and/or ligation of the pancreatic duct or duodenal or arterial occlusion. The aim of this study was to establish and characterize a noninvasive model of severe acute pancreatitis in rats. METHODS: Wistar rats were infused intravenously with cerulein or a combination of cerulein and enterokinase. Saline (154-mmol/L NaCl) or enterokinase only was infused in controls. In a first set of experiments, intrapancreatic protease activation and the release of cytokines were correlated with the severity of organ injury. Pancreatic and pulmonary injuries were determined at 6 h. In a second set of experiments, we assessed 24-h survival, serum parameters possibly reflecting the course of the disease, and morphologic changes later in the course of the disease. RESULTS: The severity of pancreatic injury and survival were correlated strongly with the amount of enterokinase infused simultaneously with cerulein. Trypsin as well as elastase and cathepsin B activity in pancreatic tissue samples were increased markedly in these animals. Marked pancreatic hemorrhage, necrosis, and leukocyte infiltration were present in animals with the greatest amounts of enterokinase infused. IL-6 and LDH, but not IL-1beta, CRP, and amylase, in serum correlated with the severity of pancreatitis. CONCLUSIONS: This noninvasive rat model of acute pancreatitis is characterized by major pancreatic necrosis, hemorrhage, and fatality. The simple and noninvasive induction technique may have advantages for future studies on inflammatory changes and sepsis in necrotizing pancreatitis compared with other currently available invasive models.     

Caerulein-induced pancreatitis and islet blood flow in anesthetized rats

BACKGROUND: Microcirculatory mechanisms have been suggested to be involved in the development of acute pancreatitis. Islet blood flow has not previously been studied in this disease. The present study aimed to investigate the effects of caerulein-induced pancreatitis on pancreatic blood perfusion, especially islet blood flow. MATERIALS AND METHODS: Continuous 4 h caerulein-infusion was used to induce mild, edemateous pancreatitis in anesthetized Sprague-Dawley rats. Some animals were then given an additional 2 h infusion of saline. Thus, at 4 or 6 h after initiating caerulein infusion the blood flow to the pancreas, pancreatic islets, and intestines was measured with a microsphere technique. RESULTS: All infused animals demonstrated an edemateous pancreatitis, without hemorrhages. Both total pancreatic and islet blood flow was increased after the 4-h infusion. However, the increase was less pronounced in the islets. After an additional 2 h with only saline infused, the blood flow values in rats initially infused with caerulein were lower than at 4 h, but total pancreatic blood was still higher than in control rats. No effects on intestinal blood flow values were seen. CONCLUSIONS: Pancreatic islet blood flow in rats with mild edematous pancreatitis is increased, but not to the same extent as that in the whole pancreas.     

Surgical Therapy of Pancreatic Pseudocysts

Background  Pancreatic pseudocysts are a common complication associated with acute and chronic pancreatitis. Fifteen percent and 40% of patients diagnosed with either acute or chronic pancreatitis, respectively, develop pseudocysts (Grace and Williamson, Br J Surg, 80:573–581, 1993). The treatment of pancreatic pseudocysts has evolved since the early 1980s, and changes in management have lead to an improved understanding of the pathophysiology of pseudocysts as well as necessary treatment paradigms. Conclusions  It has become evident that not all pseudocysts are equal. Pseudocysts arising in the setting of acute pancreatitis have a different pathophysiologic basis than those arising from chronic pancreatitis. Moreover, even those pseudocysts that arise in acute pancreatitis exhibit unique features. Pseudocysts that develop from a mild episode of pancreatitis, complicated by pancreatic duct disruption, differ significantly from those developed as a consequence of severe acute necrotizing pancreatitis with severe distortion of the pancreatic parenchyma or pancreatic duct. This review will focus on the surgical therapy of pancreatic pseudocysts in the context of the underlying pathophysiology and alternative nonoperative therapies.     

大黄对急性胰腺炎大鼠早期的治疗作用

采用胰管内逆行注入牛磺胆酸钠造成大鼠急性胰腺炎模型，造模后用中药大黄、生理盐水进行治疗，并观察治疗前后急性胰腺炎大鼠血中肿瘤坏死因子、内毒素及淀粉酶的变化，结果显示大黄组造模后２４小时后内毒素水平明显低于生理盐水组，大黄组肿瘤坏死因子、淀粉酶水平均较生理盐水组有显著降低。实验显示大黄对急性胰腺炎大鼠早期病生理改变有明显的治疗作用     

The role of biliary obstruction in the pathogenesis of acute pancreatitis in the opossum

Pancreatitis was induced in the opossum by occluding the common bile duct above or below the entrance of the pancreatic duct. The common channel theory was tested by evaluating the effect of preligation of the pancreatic duct to prevent the reflux of bile after ligation of the distal common duct. The severity of the disease was determined by histologic grading of the degree of pancreatic tissue necrosis. Serum amylase, lipase, and calcium were determined. Concomitant obstruction of the biliary and pancreatic ducts produced severe necrotizing pancreatitis whether or not bile reflux was present. Pancreatic ductal obstruction alone was associated with acinar atrophy and mild interstitial pancreatitis. Biliary obstruction alone above the entrance of the pancreatic duct resulted in marked hyperemia of the gland but without histologic evidence of pancreatic inflammation. A positive bacterial culture of the pancreas was obtained in only four of 36 opossums in a distribution to suggest random contamination. There was an inverse correlation between calcium levels and the degree of tissue necrosis. This study demonstrates that biliary obstruction rather than bile reflux into the pancreas is a requisite for the pathogenesis of severe biliary pancreatitis in this model.     

Renal microcirculation in experimental acute pancreatitis of dogs--the effect of pancreatic protease inhibitor and dopamine

To understand the renal microcirculation in acute pancreatitis is important to know the pathophysiology of renal insufficiency frequently observed as one of multiple organ failures in severe acute pancreatitis. In mongrel dogs acute pancreatitis was experimentally introduced by autologous bile added trypsin injection into the pancreatic duct. The effect of new synthesized pancreatic protease inhibitor (PATM) and dopamine in a dose of 3mg/kg/hr and 10 micrograms/kg/min were investigated, respectively. In acute pancreatitis dogs, renal arterial blood flow and renal tissue blood flow immediately fell and gradually decreased in time course of experiment and renal vascular resistance increased from 2 hours after onset of pancreatitis. When pancreatic protease inhibitor (PATM) was infused in acute pancreatitis dogs, blood pressure and pulse pressure relatively preserved during the experiment. Renal blood flow and renal tissue blood flow were maintained during the first 1 hour and thereafter slightly decreased, however which was less than that of no PATM treated dogs. When dopamine was infused in acute pancreatitis dogs, blood pressure was maintained during the first 90 minutes thereafter remarkably decreased. Renal blood flow was maintained within 60 minutes, however it remarkably decreased at the end of the experiment. This study suggested that renal microcirculation was disturbed from early period of acute pancreatitis in dogs and pancreatic protease inhibitor (PATM) had a beneficial effect of maintain the renal microcirculation.     

Problems of pancreatitis

Pancreatitis is not one disease but several and perhaps many. Diagnosis is imperfect in all forms and the usual lack of histologic material has hampered attempts to understand the pathogenesis and possible interrelationships of the different forms of pancreatic inflammation. Acute pancreatitis does not as a rule evolve into chronic pancreatitis, even after multiple recurrences. Recurrent acute attacks can be ended by identifying and treating the factor causing the disease, including recently recognized entities such as accessory papilla stenosis associated with pancreas divisum. Attempts to improve the treatment of severe acute pancreatitis are focussing upon preventing injury to pancreatic cell structures, enhancing endogenous mechanisms for capture and disposal of activated enzymes, and upon early detection and debridement of damaged pancreatic and peripancreatic tissues. Pancreatic duct stricture or obstruction as a consequence of scarring from necrotizing pancreatitis may produce recurrent symptoms, now designated as obstructive pancreatitis. Obstructive pancreatitis has its own unique histologic characteristics and is appropriately treated by resection of the blocked segment of pancreas when the point of obstruction is distal to the papilla. Chronic pancreatitis differs from acute or obstructive pancreatitis in that it is difficult or impossible to halt its progression. The role of intraductal protein precipitates, whether of enzymes or perhaps of other unique pancreatic secretory proteins, in the pathogenesis of the disease is being evaluated. The goal of surgical treatment is not to cure, but to reduce pain, overcome associated obstruction of the bile duct or duodenum, and to treat pancreatic duct disruptions including pseudocysts and internal pancreatic fistulas. Because continuing deterioration of pancreatic function is to be expected in chronic pancreatitis, maximum conservation of pancreatic tissue by avoiding resectional procedures is advisable.     

尿激酶区域动脉灌注治疗大鼠重症急性胰腺炎的实验研究

目的　探讨尿激酶区域动脉灌注 (LAI)对重症急性胰腺炎 (SAP)大鼠微循环的影响。方法　以 5 %牛磺胆酸钠胰胆管注射 (1ml/kg )制成大鼠急性胰腺炎模型 ,以生理盐水LAI为对照 ,检测血浆和全血粘度 ,观察胰腺病理变化 ,并以激光多普勒检测大鼠胰腺血流量。结果　SAP血浆和全血粘度明显升高 ,血流量下降 ,与正常组对比有显著差异 (P <0 0 5 ) ;尿激酶LAI则使SAP大鼠血浆和全血粘度降低 ,血流量上升 ,但与对照组及正常组对比均有显著差异 (P <0 0 5 )。结论　尿激酶LAI能改善SAP大鼠胰腺微循环 ,但不能完全阻止SAP的病理演变。     

Dorsal duct sphincterotomy is effective long-term treatment of acute pancreatitis associated with pancreas divisum

Nonbiliary, nonalcoholic pancreatic inflammatory disease was investigated by biochemical investigation, ultrasonography, endoscopic retrograde cholangiopancreatography, and secretin tests. Twenty-five consecutive cases were followed up for 12 months to 10 years after treatment of disease associated with pancreas divisum, diagnosed by endoscopic retrograde cholangiopancreatography. Thirteen patients had no recurrence of acute pancreatitis after dorsal duct sphincterotomy alone, during long-term follow-up (mean, 54 months); one patient had recurrent pancreatitis during 33 months after failed sphincterotomy. Eight patients had variable results 12 months to 8 years (mean, 49 months) after dorsal duct sphincterotomy for pancreatic pain syndrome (without amylase elevation), three were pain free, and one had recurrent pancreatitis. For 10 years after dorsal duct sphincterotomy for chronic pancreatitis, one patient had no pain relief; after subtotal pancreatectomy and pancreaticojejunostomy of the dorsal duct, both for chronic pancreatitis, one patient each was pain free and normoglycemic after 54 and 12 months, respectively. Dorsal duct sphincterotomy alone is successful in achieving long-term freedom from recurrence of acute pancreatitis associated with pancreas divisum. Pancreatic pain syndrome is not consistently improved by dorsal duct sphincterotomy. Chronic pancreatitis associated with pancreas divisum should be treated by resection or drainage procedures, not by dorsal duct sphincterotomy.     

Experimental model of obstructive, chronic pancreatitis in pigs

BACKGROUND: We aimed to develop a reproducible, experimental model of obstructive pancreatitis for future analysis of surgical interventions, and characterized this model using functional, histological and biochemical parameters. ANIMALS AND METHODS: In 10 female pigs the pancreatic duct (PD) was ligated. After 4, 6 or 8 weeks the animals were sacrificed. Before and after ligation, glucose tolerance and intraductal pressure were measured, and pancreatic juice was collected after stimulation with cholecystokinin and secretin. Amylase and lipase activities were analyzed in plasma and juice. Pancreatic tissue was collected for histochemical analysis. RESULTS: Within 4 weeks of ligation, the pancreas appeared atrophic. Intraductal pressure had risen significantly. Acinar-to-ductal metaplasia was accompanied by strong proliferation of stellate cells and increased collagen deposition. Islets of Langerhans appeared smaller and more numerous. Blood amylase and lipase levels were normal and glucose tolerance was unaffected. Pancreatic juice volume and amylase and lipase activities were significantly lower. CONCLUSION: Ligation of the PD in pigs resulted in a marked fibrosing obstructive pancreatitis within 4 weeks, similar to human chronic pancreatitis in regard to clinical, functional, histological and biochemical parameters.     

Systemic intravenous infusion of bovine hemoglobin significantly reduces microcirculatory dysfunction in experimentally induced pancreatitis in the rat

OBJECTIVE: To evaluate the effectiveness of bovine hemoglobin on pancreatic microcirculation and outcome in experimental acute rodent pancreatitis. SUMMARY BACKGROUND DATA: Stasis of the pancreatic microcirculation initiates and aggravates acute pancreatitis. Hydroxyethyl-starch (HES) has been shown to improve pancreatic microcirculation. Similarly, bovine hemoglobin might improve rheology due to its colloid effect, but additionally supplies oxygen to oxygen depleted pancreatic tissue. METHODS: In Wistar rats, severe acute pancreatitis was induced by administration of glucodeoxycholic acid i.d. and cerulein i.v. Pancreatic microcirculation was continuously monitored by fluorescence microscopy. Fifteen minutes after the initiation of acute pancreatitis, animals received either 0.8 mL bovine hemoglobin (Oxyglobin), HES, or 2.4 mL 0.9% NaCl i.v. at random. After 6 hours, animals were killed and histopathological damage of the pancreas was assessed using a validated histology score (0-16). RESULTS: In comparison to controls, pancreatic microcirculation improved significantly in the HBOC group (mean difference of capillary density 31.4%; standard error 5.6%; P < 0.001; 95% confidence interval for difference 17.5-45.3). HES was not as effective as HBOC substitution. The histology score revealed less tissue damage in the HBOC group [6.25 vs. 9.25 (3-8.5 vs. 8-10.75, P < 0.001)] in comparison to controls and also in comparison to the HES group [6.25 vs. 8 (3-8.5 vs. 6.5-10.25, P < 0.006)]. CONCLUSIONS: In severe acute pancreatitis, single i.v. injection of bovine hemoglobin improves pancreatic microcirculation and reduces tissue damage.     

Pancreatic capillary blood flow in an improved model of necrotizing pancreatitis in the rat

INTRODUCTION: The development of acute pancreatitis is characterized by profound changes in pancreatic microcirculation. Using in vivo microscopy with fluorescent-labeled erythrocytes as tracers we studied changes in pancreatic microcirculation in an improved rat model of necrotizing pancreatitis (NP) in comparison to edematous pancreatitis (EP) and healthy controls. METHODS: Twenty-one male Wistar rats had their pancreatae exteriorized in a temperature-controlled immersion chamber followed by intravenous administration of fluorescent-labeled autologous erythrocytes. EP was induced by intraductal saline and intravenous caerulein (5 microg/kg/h) for 6 h (n = 7) and NP by controlled intraductal infusion of glycodeoxycholic acid (10 mmol/L) followed by intravenous caerulein (n = 7). Control animals received intraductal and intravenous saline (n = 7). The determination of pancreatic microcirculation was performed before as well as 1, 3, and 6 h after intraductal infusion by correlating the number of passing labeled erythrocytes/capillary/min with their concentration per microliter of arterial blood. RESULTS: Pancreatic capillary flow in control animals remained constant over the 6-h observation period. Pancreatic capillary flow in the EP group rapidly increased to 188% of baseline after 3 h and remained significantly elevated throughout the experiments (P = 0.0001). In contrast, pancreatic capillary flow decreased significantly in the group suffering NP with values 46.7% of baseline after 6 h (P = 0.0001). Complete capillary stasis developed in 38% of investigated capillaries in the NP group compared to 0-1% in both other groups (P = 0.0001). CONCLUSION: Pancreatic microcirculation in mild edematous pancreatitis is significantly increased while the evolution of necrotizing pancreatitis in the model studied herein is characterized by a dramatic reduction in pancreatic capillary flow in conjunction with areas of capillary stasis. These results underline the pathophysiologic relevance of the model and of therapeutic measures aimed at an improvement of pancreatic microcirculation in clinical necrotizing pancreatitis.     

Reticuloendothelial system blockade promotes progression from mild to severe acute pancreatitis in the opossum

OBJECTIVE: To examine the relation between hepatic reticuloendothelial system (RES) dysfunction and the development of acute biliary pancreatitis. In an opossum model, the authors tested the hypothesis that RES blockade can turn the mild pancreatitis seen after pancreatic duct obstruction (PDO) into the severe form. SUMMARY BACKGROUND DATA: Biliary obstruction is considered the decisive event in gallstone pancreatitis. Suppression of the RES occurs during biliary obstruction. METHODS: Eighteen opossums were placed into three groups of six animals each: group A, RES blockade with lambda-carrageenan; group B, PDO; and group C, PDO and RES blockade with carrageenan. The severity of pancreatitis was evaluated by enzyme serum levels and percentage of pancreatic tissue necrosis. RES capacity was measured by dynamic liver scintigraphy, and hepatic blood flow was documented using the hydrogen clearance technique. RESULTS: No changes in hepatic blood flow occurred in groups A to C. RES capacity was suppressed in groups A and C; in group B, RES function remained unchanged. In group A, amylase and lipase levels remained normal, 3 +/- 1.9% of pancreatic tissue were necrotic. The animals in group B developed mild edematous pancreatitis with an increase in amylase and lipase levels and 15 +/- 10% of pancreatic necrosis. In group C, amylase and lipase increased significantly and histology revealed severe necrotizing pancreatitis, with 72 +/- 11% of necrotic areas. CONCLUSIONS: Artificial RES blockade can promote the progression from mild pancreatitis as observed after PDO to the severe necrotizing form of the disease. Thus, RES dysfunction resulting from biliary obstruction might be an important cofactor in the pathogenesis of bile-induced pancreatitis.     

Problems of pancreatitis

Pancreatitis is not one disease but several and perhaps many. Diagnosis is imperfect in all forms and the usual lack of histologic material has hampered attempts to understand the pathogenesis and possible interrelationships of the different forms of pancreatic inflammation. Acute pancreatitis does not as a rule evolve into chronic pancreatitis, even after multiple recurrences. Recurrent acute attacks can be ended by identifying and treating the factor causing the disease, including recently recognized entities such as accessory papilla stenosis associated with pancreas divisum. Attempts to improve the treatment of severe acute pancreatitis are focussing upon preventing injury to pancreatic cell structures, enhancing endogenous mechanisms for capture and disposal of activated enzymes, and upon early detection and debridement of damaged pancreatic and peripancreatic tissues. Pancreatic duct stricture or obstruction as a consequence of scarring from necrotizing pancreatitis may produce recurrent symptoms, now designated as obstructive pancreatitis. Obstructive pancreatitis has its own unique histologic characteristics and is appropriately treated by resection of the blocked segment of pancreas when the point of obstruction is distal to the papilla. Chronic pancreatitis differs from acute or obstructive pancreatitis in that it is difficult or impossible to halt its progression. The role of intraductal protein precipitates, whether of enzymes or perhaps of other unique pancreatic secretory proteins, in the pathogenesis of the disease is being evaluated. The goal of surgical treatment is not to cure, but to reduce pain, overcome associated obstruction of the bile duct or duodenum, and to treat pancreatic duct disruptions including pseudocysts and internal pancreatic fistulas. Because continuing deterioration of pancreatic function is to be expected in chronic pancreatitis, maximum conservation of pancreatic tissue by avoiding resectional procedures is advisable. This report is the gist of a paper read by A. L. W. at the 86th Annual Meeting of the Japanese Surgical Society, Tokyo, Japan, 1986     

胰管结石伴发慢性胰腺炎急性发作临床诊治探讨

目的 探讨胰管结石伴发慢性胰腺炎急性发作的临床治疗方案.方法 回顾性分析南华大学附属南华医院1998年1月至2006年9月收治的11例胰管结石伴发慢性胰腺炎急性发作病人的临床资料,11例均接受手术治疗,其中胰头部胰管切开加十二指肠乳头成形及胆总管切开T管引流术2例,胰管切开取石并胰管空肠Roux-en-Y吻合术5例,胰体尾切除加胰断端面胰管空肠Roux-en-Y吻合2例.单纯胰尾切除2例.结果 术后疼痛治愈率54.54%(6/11),好转率45.45%(5/11),胰漏(瘘)或出血27.27%(3/11).9例平均随访时间(39.2±36.2)个月,均无并发症出现.结论 胰管结石伴发慢性胰腺炎急性发作者早期宜非手术治疗,3个月后接受适宜的外科手术治疗,效果肯定.并发症发生率较低,术式根据结石部位、主胰管是否通畅决定.     

Post-ERCP acute necrotizing pancreatitis

An analysis of acute necrotizing pancreatitis (ANP) after endoscopic retrograde cholangiopancreatography (ERCP) was carried out. The incidence of ANP was 0.5% (5/914) for ERCP and 0.5% (2/370) for endoscopic sphincterotomies (EST). All the five patients were obese, middle-aged or older women. Four had a suspicion of common bile duct stones and the fifth a pancreatic tumour as an indication for ERCP. Two had most probably a functional sphincteric disorder and the third was without clear pathological findings. In the remaining two cases the bile duct cannulation failed and repeated pancreatic duct cannulation occurred; while in one case the pancreatic duct was not cannulated. The four pancreatographies were normal and without parenchymal opacification. Symptoms of acute pancreatitis started within 6 hours after ERCP. The pancreatitis was severe by Ranson criteria and necrotizing by evaluation at laparotomy. All the patients showed bacterial growth either in bile, blood or ascitic fluid early in the course of pancreatitis (E. coli, Str. faecalis or Klebsiella pneumoniae). The possible pathogenetic factors of post-ERCP ANP are discussed.     

Early management of traumatic pancreatic transection by spleen-preserving laparoscopic distal pancreatectomy

Pancreatic trauma is a common cause of acute pancreatitis in children and is often treated by conservative measures alone. Conservative measures are more likely to fail when there is complete pancreatic duct disruption. We report a case of complete transaction of the pancreatic neck following blunt trauma in a 14-year-old boy. Complete duct disruption was confirmed by endoscopic retrograde pancreatography. The patient was successfully managed by a laparoscopic spleen-preserving distal pancreatectomy and recovered quickly without complications. The merit of a laparoscopic approach to severe pancreatic injury in children is discussed.