Pancreatic Duct Pressure Research Articles

Coexistence of acute pancreatitis and an obstructing upper ureteral calculus: does a calculus cause pancreatitis? a case report.

A 36-year-old male patient presented with epigastric, and right loin pain with decreased urine output for 3 days. On physical examination, he had central abdominal and right flank tenderness. An abdominal ultrasound showed mild to moderate ascites, a hyperechoic pancreas, a small (26×77mm) left kidney with increased echogenicity, right renal hypertrophy with moderate hydronephrosis, and a dilated upper ureter due to a 10mm obstructing stone with a perirenal fluid collection. The diagnosis of acute pancreatitis with an obstructing right upper ureteric stone was established. Under spinal anesthesia, an emergency ureteroscopy with laser fragmentation of the stone was performed, and a JJ stent was inserted. He developed postobstructive diuresis and his renal function was improved with a rapid decline of pancreatic enzymes as well. Two theories explain the presentation of acute pancreatitis by ureteral obstruction. First, the obstructed severe hydronephrotic kidney compresses the duodenum and head of the pancreas, obstructing the distal part of the common bile duct and triggering the elevation of pancreatic duct pressure, bile reflux, trypsin activation, and pancreatic autodigestion. The second theory states that acute pancreatitis develops when urine is extravasated from an obstructed kidney into the adjacent tissues, irritating the uncinate process of the pancreas. Although mentioning ureteral obstruction as a cause of pancreatitis is scarce, the clinician should be aware that in each case of ureteral obstruction, the emergence of acute pancreatitis is a possible complication.

Association of postoperative opioid use with pancreatic fistula rates after distal pancreatectomy

Background: The rate of clinically relevant postoperative pancreatic fistula (CR-POPF) after distal pancreatectomy ranges from 15-35% in the literature. Many risk factors have been reported with no consensus on their predictive value. Prior studies have observed an association between increased postoperative opioid use and fistula formation, secondary to increased sphincter of Oddi tone that leads to impaired emptying and increased pancreatic duct pressure. Our group has implemented perioperative care pathways, with each iteration increasingly using non-opioid medication bundles and reducing administered opioids. The aim of this study was to determine the association between perioperative variables, including early postoperative opioid use, and CR-POPF.

Wirsungectomy for pancreatic hypertension in chronic pancreatitis

Background. Pain in chronic pancreatitis (CP) can occur as a consequence of mechanical factors— pancreatic ductal hypertension, interstitial pressure, inflammatory and neuropathic pathological changes in the pancreas. The purpose was to evaluate a novel modification of the classic Partington-Rochelle procedure via comparing functional results of conventional surgery group and wirsungectomy group. Materials and methods. A retrospective analysis of the case histories of patients with CP and an enlarged (≥4mm) main pancreatic duct was carried out for the period from 2003 to 2009, which underwent surgical treatment of CP. The SF-36 and EORTC QLQ-C30 questionnaires, and visual analogue scale of pain were used for the assessment. The first group included five patients with wirsungectomy with lateral pancreaticojejunostomy (PEA + WE); the second group consisted of 20 patients after the lateral pancreaticojejunostomy (PEA) only. Cross-tabulation analyses were performed to compare PEA and PEA + WE groups as well as those groups in different time points using a two-sided Student’s t-test. The significance level was set to p<0.05. Results. The groups were compared in terms of VAS and the EORTC QLQ-C30 questionnaire before and 2 years after surgery using Student’s t-test for unrelated values: statistically significant differences between the groups according to VAS as before (p=0.757) and after surgery (p=0.696) were not obtained. There were no significant differences (p > 0.05) between the PEA and PEA + WE groups before and after surgery according to the EORTC QLQ-C30 questionnaires, except for some items (p<0.05) Within the groups according to VAS and EORTC QLQ-C30 (pain severity), in the PEA group (p=0.000001, p=0.000109) and the PEA + WE group (p=0.018, p=0.017) after surgery, there was a statistically significant decrease in pain. Conclusions. Longitudinal pancreaticojejunostomy with wirsungectomy is justified in patients with long-term CP, severe fibrosis of the pancreas with multiple calcifications of the periphery pancreatic ducts to decompress pancreatic ducts, and parenchyma. In the long-term period after 2 years, the proposed method of longitudinal pancreaticojejunostomy with wirsungectomy in patients with CP with dilation of main pancreatic duct according to the VAS scale and EORTC QLQ questionnaires C30 and SF-36 is accompanied by a significant reduction in pain.

Piezo1-mediated stellate cell activation causes pressure-induced pancreatic fibrosis in mice.

Pancreatic fibrosis is a complication of chronic pancreatitis and is a prominent feature of pancreatic cancer. Pancreatic fibrosis is commonly observed in patients with prolonged pancreatic duct obstruction, which elevates intrapancreatic pressure. We show here that increased pancreatic duct pressure causes fibrosis and describes the mechanism by which pressure increases deposition of extracellular matrix proteins and fibrosis. We found that pancreatic stellate cells (PSCs), the source of the extracellular matrix proteins in fibrosis, express the mechanically activated ion channel Piezo1. By increasing intracellular calcium, mechanical stress or the Piezo1 agonist Yoda1-activated PSCs manifest by loss of perinuclear fat droplets and increased TGF-β1, fibronectin, and type I collagen expression. These effects were blocked by the Piezo1 inhibitor GsMTx4 and absent in PSCs from mice with conditional genetic deletion of Piezo1 in stellate cells, as was pancreatic duct ligation–induced fibrosis. Although TRPV4 has been proposed to have direct mechanosensing properties, we discovered that PSCs from Trpv4-KO mice were protected against Yoda1-triggered activation. Moreover, mice devoid of TRPV4 were protected from pancreatic duct ligation–induced fibrosis. Thus, high pressure within the pancreas stimulates Piezo1 channel opening, and subsequent activation of TRPV4 leads to stellate cell activation and pressure-induced chronic pancreatitis and fibrosis.

Chronic pancreatitis is an acid dependent disease. Which mark to put at the end of the sentence: interrogative, exclamation, dot or ellipsis?

Chronic pancreatitis (CP) is one of the most widespread gastroenterological diseases, the pathogenic mechanisms of which are still under investigation. The authors gave a short overview of the main stages in the research of the relationships between gastric and pancreatic secretion, and the results of physiological studies, performed by I. P. Pavlov and his students. Being а strict follower of «nervousness» theory, the great physiologist and his associates made the incorrect conclusions about the presence of local nerve connections (peripheral reflex arc) between the duodenum and pancreas, not suggesting the presence of humoral interactions. The modern data have been presented that give the evidence that duodenal acidification results in the secondary deficiency of endogenous pancreatic enzymes, increased stimulation of pancreatic secretion, exacerbated symptoms of exocrine pancreatic insufficiency, increased secretory tension in pancreatic tissue, duct and tissue pressure, and increased risk of CP attack.However, a dot at the end of a statement «CP is an acid-dependent disease» is tentative. The proton pump inhibitors (PPIs) are used throughout for the treatment of acid-dependent diseases. However, neither European, nor Russian recommendations do include PPIs as a basic treatment for CP. The results of a prospective randomized controlled trial, which proved the effectiveness of CP treatment with the use of combination of analgesics and PPIs have been considered. However, the results of the only study are not enough to recommend the inclusion of PPI in the basic CP therapy. The analysis has been performed for the provisions of the European Guidelines for the Diagnosis and Treatment of Pancreatitis. These guidelines describe situations when PPIs should be included in the complex CP treatment. The data of evidence-based medicine have been presented, illustrating that suppression of gastric secretion can increase the effectiveness of enzyme preparations in comparison with the administration of pancreatin monotherapy. The advantages of pantoprazole among other of the PPIs’ representatives have been analyzed. A clinical case of CP treatment with a reasonable pantoprazole (Nolpaza) administration have been considered.

Hypoxia of pancreas in pathogenesis of fibrosis in chronic pancreatitis

The pathogenesis of chronic pancreatitis and pain syndrome had not been fully studied. The aim of the study was to evaluate the interrelation of fibrotic and ischemic changes in the parenchyma of pancreas, and pancreatic duct pressure in the pathogenesis of chronic pancreatitis. In a prospective study, a morphological, the immunohistochemical study of pancreatic preparations was performed, and the indicators of tissue oximetry and pancreatic duct pressure were studied intraoperatively in 40 patients operated for chronic pancreatitis. It was found that with the progression of fibrotic changes in the pancreatic tissue of patients with chronic pancreatitis, there was an increase in TGF-β1 expression (р < 0.001), an increase in the number of pancreatic stellate cells (r = 0.32, р < 0.05), a decrease in glycogen (ischemia marker). The intraoperative direct measurement revealed a high pancreatic duct pressure: 34.2 (26.6; 45.3) mm Hg, a decrease in oxygenation of the pancreatic tissue that correlate with a degree of fibrosis. The pancreatic tissue in chronic pancreatitis has chronic hypoxia associated with fibrosis and increased pancreatic ductal hypertension. So, secondary pancreatic ischemia can be a significant factor in the progression of fibrosis and chronic pain syndrome in chronic pancreatitis.

Single-needle celiac plexus block for pain management in a case of liver hemangioma

Pain is the most common reason for presentation of a patient to a physician suffering from upper abdominal pathologies such as pancreatitis, benign tumors, or malignancies of liver/gall bladder/stomach/colon. Inflammation, scarring, and increased pancreatic duct pressure or malignant invasion of celiac plexus are the major causes of pain. A comprehensive evaluation of the patient for pain, associated pathological problem, and to find out any surgical indication is necessary. We present a 55-year-old female patient diagnosed of liver hemangioma with right upper abdominal pain. Treatment options of embolization under radiological guidance and/or surgical resection–enucleation were not acceptable and affordable to the patient. The patient was then referred for upper right intra-abdominal pain management. Following informed consent and vital monitoring inside the operation theater, the patient was given prone position. Under aseptic precautions and fluoroscopy guidance, diagnostic celiac plexus block was given on the right side with 5 ml of 2% lignocaine with adrenaline + 20 ml of 0.25% bupivacaine + fentanyl 25 μg at the level of L1 body of vertebra, which resulted in 80% of relief in pain for 18 h. Later, this was followed by neurolytic block using 15 ml of 8% phenol after injection of 10 ml of 0.25% bupivacaine to confirm the effective pain relief. Numerical Rating Scale score decreased from 7 to 2 at 1 week. Seventy-five percent of pain relief was present at the 6th month of follow-up. There was significant improvement in quality of life and sleep. Single-needle technique of celiac plexus block is a useful method for the control of chronic upper abdominal pain due to liver pathology.

Algorithm of surgical treatment of complicated forms of chronic pancreatitis.

The purpose of the work was to evaluate the algorithm of surgical treatment of complicated forms of chronic pancreatitis. The results of surgical treatment of 181 patients with complicated forms of chronic pancreatitis were analyzed. 24.5% of patients were admitted with type B pain syndrome. Among them, all patients had multiple strictures of the main pancreatic duct and tissue pressure resistance was >200 mm Hg. Histologically,these patients had stage 4 of pancreatic fibrosis. A combined local resection by Frey-Izbickiy allows to reduce the number of relapses of pancreatic hypertension by 11.1%.

Risk of pancreatitis after pancreatic duct guidewire placement during endoscopic retrograde cholangiopancreatography.

Background & aimsAdvanced techniques have been developed to overcome difficult cannulation cases in endoscopic retrograde cholangiopancreatography (ERCP). Pancreatic duct guidewire placement method (PGW) is performed in difficult cannulation cases; it is possible that it places patients at risk of post-ERCP pancreatitis (PEP). The mechanism of PEP is still unclear, but pancreatic duct pressure and injury of pancreatic duct are known causes of PEP. Therefore, we hypothesized a relationship between pancreatic duct diameter and PEP and predicted that PGW would increase the risk of PEP in patients with non-dilated pancreatic ducts. This study aimed to investigate whether PGW increased the risk of PEP in patients with pancreatic duct diameter ≤ 3 mm.MethodsWe analyzed 332 patients with pancreatic duct ≤ 3 mm who performed first time ERCP session. The primary endpoint was the rate of adverse event of PEP. We evaluated the risk of PEP in patients who had undergone PGW compared to those who had not, using the inverse probability of treatment weighting (IPTW) analysis.ResultsPGW was found to be an independent risk factor for PEP by univariate analysis (odds ratio [OR], 2.45; 95% confidence interval [CI], 1.12–5.38; p = 0.03) after IPTW in patients with pancreatic duct diameter ≤ 3 mm. Adjusted for all covariates, PGW remained an independent risk factor for PEP (OR, 3.12; 95% CI, 1.33–7.33; p = 0.01).ConclusionOur results indicate that PGW in patients with pancreatic duct diameter ≤ 3 mm increases the risk of PEP.

Management of pain in chronic pancreatitis with emphasis on exogenous pancreatic enzymes.

One of the most challenging issues arising in patients with chronic pancreatitis is the management of abdominal pain. Many competing theories exist to explain pancreatic pain including ductal hypertension from strictures and stones, increased interstitial pressure from glandular fibrosis, pancreatic neuritis, and ischemia. This clinical problem is superimposed on a background of reduced enzyme secretion and altered feedback mechanisms. Throughout history, investigators have used these theories to devise methods to combat chronic pancreatic pain including: Lifestyle measures, antioxidants, analgesics, administration of exogenous pancreatic enzymes, endoscopic drainage procedures, and surgical drainage and resection procedures. While the value of each modality has been debated over the years, pancreatic enzyme therapy remains a viable option. Enzyme therapy restores active enzymes to the small bowel and targets the altered feedback mechanism that lead to increased pancreatic ductal and tissue pressures, ischemia, and pain. Here, we review the mechanisms and treatments for chronic pancreatic pain with a specific focus on pancreatic enzyme replacement therapy. We also discuss different approaches to overcoming a lack of clinical response update ideas for studies needed to improve the clinical use of pancreatic enzymes to ameliorate pancreatic pain.

Accessory pancreatic duct patterns and their clinical implications.

Accessory pancreatic duct (APD) designed to reduce the pressure of major pancreatic duct by forming a secondary drainage channel. Few studies have mentioned the variant types of accessory ducts and their mode of formation, some of these have a clear clinical significance. Present study is aimed to evaluate the possible variations in the APD and its terminations. Forty formalin fixed adult human pancreas with duodenum in situ specimens were studied by injecting 1% aqueous eosin, followed by piece meal dissection of the head of the pancreas from posterior surface. Formation, tributaries, relations, and the termination of the accessory pancreatic duct were noted and photographed. Accessory ducts revealed 50% belonged to long type, 22.5% were of short and ansa pancreatica type each, and embryonic type of duct pattern was seen in 5% specimens. 75% of long type ducts showed positive patency with eosin dye, followed by ansa type (44.4%), and least patency was found in short type (22.2%). With regard to the patency of the accessory pancreatic ducts towards their termination, we found 52.5% of the accessory ducts and 5% of the embryonic type pancreatic ducts were patent and in 42.5% of the specimen the ducts were obliterated. In 85% of specimens the minor duodenal papillae was anterosuperior to the major papilla and superior to the major papillae in 10% of the cases, and in 5% minor papillae was absent. The average distance between the two papillae was 2.35 cm. The knowledge of the complex anatomical relations of the gland with its duct, duodenum and bile ducts are essential for the surgeons and sinologists to plan and perform both the diagnostic as well as therapeutic procedures effectively.

Acinarization (parenchymal blush) observed during secretin-enhanced MRCP: clinical implications.

T2 hyperintensity of pancreatic acini during secretin-enhanced MRCP is called "acinarization." We sought to determine the clinical significance of this finding. Patients were selected if the radiology report included the phrases "acin*" (where * represented a wild card search) or "blush" using the institution's customized lexicon-search software. Sixty-seven consecutive patients without acinarization on secretin-enhanced MRCP who also underwent ERCP were enrolled as the control group. The intensity of acinarization was classified into three groups: grade 0, no visible acinarization; grade 1, barely visible parenchymal hyperintensity; or grade 2, easily visible parenchymal hyperintensity. ERCP findings of ductal abnormalities and basal pancreatic sphincter manometry were recorded. There were higher frequencies of divisum (p = 0.001) and of a clinical history of recurrent acute pancreatitis (p < 0.001) and higher basal pancreatic sphincter of Oddi manometric pressure measurements (p = 0.008) in the acinarization group. There was no difference in the frequency of ERCP-defined chronic pancreatitis (p = 0.10) between the groups. In patients with acinarization, a higher mean sphincter pressure was seen in patients with more intense acinarization than in those with faint acinarization, but this difference was not significant (p = 0.22). Ampullary tumors were found in four patients with acinarization. Acinarization probably occurs in patients with a propensity for increased pancreatic ductal pressure (i.e., patients with divisum, elevated basal pancreatic sphincter pressure, ampullary tumor) and adequate exocrine function (absence of severe chronic pancreatitis).

New developments in diagnosis and non‐surgical treatment of chronic pancreatitis

Chronic pancreatitis is progressive and irreversible, leading to digestive and absorptive disorders by destruction of the exocrine pancreas and to diabetes mellitus by destruction of the endocrine pancreas. When complications such as pancreatolithiasis and pseudocyst occur, elevated pancreatic ductal pressure exacerbates pain and induces other complications, worsening the patient's general condition. Combined treatment with extracorporeal shock-wave lithotripsy and endoscopic lithotripsy is a useful, minimally invasive, first-line treatment approach that can preserve pancreatic exocrine function. Pancreatic duct stenosis elevates intraductal pressure and favor both pancreatolithiasis and pseudocyst formation, making effective treatment vitally important. Endoscopic treatment of benign pancreatic duct stenosis stenting frequently decreases pain in chronic pancreatitis. Importantly, stenosis of the main pancreatic duct increases risk of stone recurrence after treatment of pancreatolithiasis. Recently, good results were reported in treating pancreatic duct stricture with a fully covered self-expandable metallic stent, which shows promise for preventing stone recurrence after lithotripsy in patients with pancreatic stricture. Chronic pancreatitis has many complications including pancreatic carcinoma, pancreatic atrophy, and loss of exocrine and endocrine function, as well as frequent recurrence of stones after treatment of pancreatolithiasis. As early treatment of chronic pancreatitis is essential, the new concept of early chronic pancreatitis, including characteristics findings in endoscopic ultrasonograms, is presented.

Endoscopic transpapillary pancreatic stenting for internal pancreatic fistula with the disruption of the pancreatic ductal system

BackgroundInternal pancreatic fistula (IPF) is a well-recognized complication of pancreatic diseases. Although there have been many reports concerning IPF, the therapy for IPF still remains controversial. We herein report our experiences with endoscopic transpapillary pancreatic stent therapy for IPF and evaluate its validity. MethodSix patients with IPF who presented at our department and received endoscopic transpapillary pancreatic stent therapy were investigated, focusing on the clinical and imaging features as well as treatment strategies, the response to therapy and the outcome. ResultsAll patients were complicated with stenosis or obstruction of the main pancreatic duct, and in these cases the pancreatic ductal disruption developed distal to the areas of pancreatic stricture. The sites of pancreatic ductal disruption were the pancreatic body in five patients and the pancreatic tail in one patient. All patients received endoscopic stent placement over the stenosis site of the pancreatic duct. Three patients improved completely and one patient improved temporarily. Finally, three patients underwent surgical treatment for IPF. All patients have maintained a good course without a recurrence of IPF. ConclusionEndoscopic transpapillary pancreatic stent therapy may be an appropriate first-line treatment to be considered before surgical treatment. The point of stenting for IPF is to place a stent over the stenosis site of the pancreatic duct to reduce the pancreatic ductal pressure and the pseudocyst's pressure.

After Distal Pancreatectomy Pancreatic Leakage from the Stump of the Pancreas May Be Due to Drain Failure or Pancreatic Ductal Back Pressure

HypothesisThe method to lower postoperative pancreatic fistula (POPF) after distal pancreatectomy (DP) involves controlling risk factors for leakage from the pancreatic stump. GoalThe aim of this study was to identify controllable risk factors for POPF. MethodsIn order to promote homogeneity, we used a single surgeon case series and then calculated POPF with a public web-based tool based on the severity classification system of the International Study Group of Pancreatic Surgery (ISGPS). A total of 223 consecutive cases of DPs were reviewed. DP involved the same hand-sewn fish-mouth closure of the pancreatic stump. All received postoperative epidural anesthesia. Logistic regression analysis identified risk factors for clinically relevant POPF (grade B/C). ResultsMortality was zero. ISGPS gradings were: no POPF 53%, grade A = 32%, B = 13.9%, and C = 0.9%. The clinical-relevant POPF (B/C) rate was 14.8% of which 24% represented surgical drain failure due to lack of patency and/or misplaced from their original location. Preoperative endoscopic ablation and/or stenting of Wirsung’s duct was a significant risk factor to lower grade B/C leak (3%). Multivariate analysis identified two controllable risk factors—intraoperative blood loss >1,000 ml and those who did not undergo preoperative endoscopic interventions of Wirsung’s duct. In the group with presumed intact pancreatic sphincters (no endoscopic intervention, n = 177), the use of postoperative intravenous opioids (with epidural failure) was a risk factor for B/C leak (34%). These findings suggest that increased back pressure in the pancreatic duct has a role in promoting pancreatic stump leakage. ConclusionsUsing the ISGPS definition and its web-based tool, the incidence of clinically relevant leakage was 14.8% in 223 cases of DP. Opportunities to lower this rate are improving our surgical drain technology, limiting intraoperative blood loss, and avoiding postoperative intravenous narcotics with epidural analgesia.

Infusion combined with duct ligation inducing acute pancreatitis in rats

Objective To establish a new acute necrotizing pancreatitis model in rats. Methods We designed single pancreatic bile duct ligation and double pancreatic bile duct ligation in rats, combined with retrogradely infusing 2% glycodeoxycholic acid ( GDCA), to test duct pressure and observe the severity of acute pancreatitis at 8, 16 and 24 h, respectively. Results In two groups, the duct pressures were (20. 60 ± 1.51 ) cm H2O and (29. 37 ±0. 87) cm H2O, respectively. Both of the two methods could induce typical acute necrotizing pancreatitis at 24 h, the severity of which progressively developed with time course(P ＜0. 01 ), at each time point, the severity of double duct ligation group was higher than single duct ligation group ( P ＜ 0. 01 ). Conclusion Retrogradely infusing 2% GDCA with constant pressure,combined with the two methods of pancreatic bile duct ligation, coude induce clinically relevant acute necrotizing pancreatitis in rats; the pancreatic duct pressure and its duration might be closely related to the arising and developing of acute pancreatitis. Key words: Acute pancreatitis; Duct ligation; Infusion

Pancreatic Duct Disruption With Autosplenectomy

Question: A 64-year-old male patient visited our cardiovascular outpatient department for regular follow-up for hypertension and coronary artery disease on July 24, 2008. Hypotension was noted; his systolic and diastolic blood pressure of 89 and 34 mmHg, respectively. So he was referred to our emergent department (ED) for further evaluation. According to his previous medical records, he had a past history of gallbladder stones inducing acute pancreatitis with pseudocyst formation over the pancreatic tail region, which was initially managed by pigtail tube drainage initially on March 21, 2008 (Figure A). Endoscopic retrograde cholangiopancreatography (ERCP) revealed pancreatic duct disruption on April 25, 2008. Hence, endoscopic papillotomy, common bile duct stone extraction and 7-French (Fr) plastic stent pancreatic duct insertion were subsequently performed. Antibiotics were prescribed and the patient was examined by abdominal sonography every week until the pseudocyst completely resolved. The pigtail drainage tube was removed when there was no further drainage and he was discharged on July 3, 2008. In our ED, the physical examination did not reveal any fever, abdominal pain, jaundice, or other specific discomfort. Blood counts were as follows: white blood cell 32,900/mm3 (normal, 4800–10,800/mm3); hemoglobin, 12.5 g/dL (normal, 12–16); and platelets, 613,000/mm3 (normal, 130,000–400,000/mm3). The differential count of white blood cell was neutrophils, 74%; lymphocyte, 19%; monocyte, 7%; eosinophils, 0%; and basophils, 0%. Serum biochemistry test results were as follows: alanine aminotransferase, 78 IU/L (normal, 0–40); alkaline phosphatase, 175 U/L (normal, 10–100); γ-glutamyltransferase, 223 U/L (normal, 8–61); total bilirubin, 0.4 mg/dL (normal, 0.2–1.6); C-reactive protein, 11.79 mg/dL (normal, 0–0.5); and amylase, 218 U/L (normal, <180). An abdominal computed tomography (CT) scan in our ED is shown in Figures B and C. Pigtail drainage and antibiotics treatment were given immediately. A pus-like discharge was found from the pig-tail drainage tube. What is the possible diagnosis? See the Gastroenterology web site (www.gastrojournal.org) for more information on submitting your favorite image to Clinical Challenges and Images in GI. Under the impression that the patient had persistent pancreatic duct disruption with autosplenectomy, ERCP was performed and the 7-Fr internal stent was replaced by an 8-Fr stent to decrease pancreatic duct pressure. The pigtail drainage tube was reimplanted from the pseudocyst to the pancreatic tail duct and gradually changed to a smaller size. However, persistent leukocytosis and thrombocytosis without clinical evidence of infectious disease were noted during this hospitalization. We consulted a hematologist and genetic studies showed mixed polyclonal blood cell counts. Hence, lymphoproliferative disease was less likely. Consequently, both functional and anatomic destruction of the spleen were highly suspected. Follow-up ERCP on October 22, 2008, disclosed a healed pancreatic duct (Figure D). Therefore, the external drainage tube was removed smoothly. Follow-up CT scan disclosed no recurrence of the pseudocyst and mild regeneration of spleen on February 22, 2009 (Figure E). The final diagnosis was pancreatic duct disruption with persistent pancreatic fluid leakage and splenic autodigestion. Autosplenectomy has been reported in a number of diseases, such as sickle cell anemia, idiopathic thrombocytopenic purpura, systemic lupus erythematosus, rheumatoid arthritis, celiac disease, amyloidosis, and splenic irradiation.1Caro J. Hypersplenism and hyposplenism.in: Lichtman M.A. Beutler E. Kipps T.J. Williams hematology. 7th ed. McGraw-Hill Medical, New York2006Google Scholar In acute pancreatitis, pseudocyst direct invasion or splenic vessel thrombosis with subsequent liquefaction of a splenic infarction are the causes of splenic parenchymal destruction.2Hastings O.M. Jain K.M. Khademi M. et al.Intrasplenic pancreatic pseudocyst complicating severe acute pancreatitis.Am J Gastroenterol. 1978; 69: 182-186PubMed Google Scholar In this case, CT scan disclosed pancreatic tail and splenic abscess without pseudocyst formation or splenic vessel thrombosis. Therefore, autosplenectomy was caused by persistent pancreatic fluid leak and local abscess formation. This case also disclosed mild splenic regeneration after autodigestion. Splenic autodigestion should be taken into consideration when duct disruption occurs at pancreatic tail. Acute pancreatitis with splenic involvement often required aggressive treatment, including repeated percutaneous drainage, pancreatectomy, and/or splenectomy.3Heider R. Behrns K.E. Pancreatic pseudocysts complicated by splenic parenchymal involvement: results of operative and percutaneous management.Pancreas. 2001; 23: 20-25Crossref PubMed Scopus (38) Google Scholar Although splenic autodigestion is rare, it may be lethal if undiagnosed. Clinicians should maintain a high index of suspicion of splenic autodigestion when patients had acute pancreatitis history with persistent leukocytosis and thrombocytosis.

Patients with Atypical Sphincter of Oddi Dysfunction Symptoms Can Benefit from Endoscopic Biliary Manometry

Introduction: Sphincter of Oddi dysfunction (SOD) is a clinical syndrome of biliary or pancreatic obstruction related to mechanical or functional abnormalities of the sphincter of Oddi. Diagnosis of SOD is usually established by endoscopic biliary manometry (EBM) performed at the time of ERCP and measures the biliary and pancreatic sphincter pressures. Depending on the results it can determine which treatments such as endoscopic sphincterotomy or Botulinum toxin injection should be given. However, the Rome III guidelines, developed for the investigation of patients with SOD, propose that unless patients meet all the criteria then they should not undergo invasive investigations such as EBM. These patients may present with a variety of symptoms which may be biliary, pancreatic, mixed or atypical in nature and this may make diagnosis difficult without doing EBM. Aims and Methods: The Royal London Hospital is a tertiary referral centre for this condition and this study was a retrospective audit of patients referred here for the investigation of SOD and who underwent EBM. It involved patients who had EBM from 1st January 2004 to 31st July 2008 and looked at the long term outcomes and complication rates. Results: 131 patients (104 females) underwent EBM during this period. 60 patients had biliary symptoms, 21 had pancreatic, 23 had mixed biliary and pancreatic and 27 had atypical abdominal symptoms. Overall 63% of patients had some improvement and long term no-one had worsening of symptoms post EBM. The Rome III guidelines do not include atypical patients for the investigation of SOD. However in our study, 11 patients in the atypical group had elevated biliary or pancreatic duct pressure (>40 mm Hg) of which 6 underwent sphincterotomy and 9 patients had ampullary Botulinum toxin injection. 11 of the atypical patients showed some improvement following EBM. In the atypical group 2 patients developed post-ERCP pancreatitis and 1 patient suffered a fatal guide wire perforation. In total 19 patients developed post-ERCP pancreatitis (12 following sphincterotomy and 5 post-Botulinum toxin injection) and 5 patients developed perforation. Conclusions: Rome III guidelines for the diagnosis of SOD are unnecessarily restrictive and therefore may lead to the under-diagnosis and treatment of this condition. Many patients, who may not fit these criteria, including those with atypical symptoms, may potentially benefit from undergoing EBM and endoscopic treatments.

Acute pancreatitis: Etiology and common pathogenesis

Acute pancreatitis is an inflammatory disease of the pancreas. The etiology and pathogenesis of acute pancreatitis have been intensively investigated for centuries worldwide. Many causes of acute pancreatitis have been discovered, but the pathogenetic theories are controversial. The most common cause of acute pancreatitis is gallstone impacting the distal common bile-pancreatic duct. The majority of investigators accept that the main factors for acute billiary pancreatitis are pancreatic hyperstimulation and bile-pancreatic duct obstruction which increase pancreatic duct pressure and active trypsin reflux. Acute pancreatitis occurs when intracellular protective mechanisms to prevent trypsinogen activation or reduce trypsin activity are overwhelmed. However, little is known about the other acute pancreatitis. We hypothesize that acute biliary pancreatitis and other causes of acute pancreatitis possess a common pathogenesis. Pancreatic hyperstimulation and pancreatic duct obstruction increase pancreatic duct pressure, active trypsin reflux, and subsequent unregulated activation of trypsin within pancreatic acinar cells. Enzyme activation within the pancreas leads to auto-digestion of the gland and local inflammation. Once the hypothesis is confirmed, traditional therapeutic strategies against acute pancreatitis may be improved. Decompression of pancreatic duct pressure should be advocated in the treatment of acute pancreatitits which may greatly improve its outcome.

Endoscopic treatment of pancreatic fistulas

Aims: Pancreatic fistula is a serious complication of acute and chronic pancreatitis or pancreatic trauma and surgery. Its management is still controversial. Patients and methods: 8 patients with pancreatic fistula were treated endoscopically over a period of 5 years. 5 patients were presented with pancreatic ascites following pancreatic tail resection (2 cases), nephrectomy (1 case), blunt abdominal trauma (1 case) and necrosectomy due to acute necrotic pancreatitis (1 case). In 1 patient pancreatic ascites and left pleural effusion developed after splenectomy and in 1 patient pleural effusion occurred as a complication of chronic pancreatitis; 1 patient had an external fistula associated with pancreatic tail pseudocyst following distal pancreatectomy. The level of amylase in the aspirated fluids were consistently elevated. The mean fistula output volume was 150ml/day. ERCP identified leaks. Dual or pancreatic sphincterotomy, pancreatic stent or nasopancreatic drain placement was performed to lower the pancreatic duct pressure and bypass the ductal disruption. Results: Dual or pancreatic sphincterotomy was effective for the 5 patients in whom the ductal injury originated from the tail of the pancreas and hence could not be bypassed (splenectomy, nephrectomy, abdominal trauma, two postoperative fistulas). These patients had no strictures in the main pancreatic duct. Their fistulas closed within 3 weeks, except for one patient whose fistula closed after 12 weeks. Pancreatic stent or nasopancreatic drain placement was performed in 3 patients with chronic pancreatitis and main pancreatic duct stricture to bypass the disruption. Only in one of the patients it was effective, leading to closure of the fistula. Endoscopic therapy was unsuccessful in 2 patients in spite of pancreatic stent, enteral nutrition and use of octreotide. They required surgery. There was no serious complication or procedure-related mortality. Conclusion: Endoscopic treatment is an effective and safe method for pancreatic fistulas, especially for patients without strictures in the main pancreatic duct.