[Evaluation of the function of the gallbladder and Oddi's sphincter by cholescintigraphy. New concept of vesicosphincter dysfunction].
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Acute pancreatitis develops immediately after the causative impulse, while chronic pancreatitis develops after the long-term action of the noxious agent. A typical representative of acute pancreatitis is biliary pancreatitis, chronic pancreatitis develops in alcoholism and has a long latency. As alcoholic pancreatitis is manifested at first as a rule by a potent attack, it is classified in this stage as acute pancreatitis. The most frequent etiological factors in our civilization are thus cholelithiasis and alcoholism (both account for 20-50% in different studies). The assumed pathogenetic principles in acute biliary pancreatitis are the common canal of both efferent ducts above the obturated papilla, duodenopancreatic reflux and intrapancreatic hypertension. A detailed interpretation is however lacking. The pathogenesis of alcoholic pancreatitis is more complicated. Among others some part is played by changes in the calcium concentration and fusion of cellular membranes. Idiopathic pancreatitis occurs in up to 10%, part of the are due to undiagnosed alcoholism and cholelithiasis. Other etiologies are exceptional. Similarly as in cholelithiasis pancreatitis develops also during other pathological processes in the area of the papilla of Vater such as dysfunction of the sphincter of Oddi, ampulloma and juxtapapillary diverticulum, it is however usually mild. The incidence of postoperative pancreatitis is declining. Its lethality is 30% and the diagnosis is difficult. In the pathogenesis changes of the ion concentration are involved, hypoxia and mechanical disorders of the integrity of the gland. Pancreatitis develops in association with other infections--frequently in mumps, rarely in hepatitis, tuberculosis, typhoid and mycoses. Viral pancreatitis is usually mild. In parasitoses pancreatitis develops due to a block of the papilla Vateri. In hyperparathyroidism chronic pancreatitis is more likely to develop, recent data are lacking. As to dyslipoproteinaemias, pancreatitis develops in the Ist, IVth and Vth type of Frederikson's classification, in rare recessive disorders and other conditions such as hypothyroidism, renal insufficiency, oestrogen substitution and others. In pancreas divisum chronic pancreatitis is more likely to develop. In exotic countries tropical pancreatitis is most frequent. It is however similarly as alcoholic pancreatitis primarily chronic. A very serious course is usual in traumatic pancreatitis. Risk factors of pancreatitis after ERCP are in particular undilated biliary pathways, dysfunction of the sphincter of Oddi and the use of a needle knife (bistoury). Medicamentous prevention is not substantiated. Drug induced pancreatic damage is much rarer than hepatotoxicity. Pancreatitis is caused most frequently by immunosuppressives, methyldopa, corticoids and oestrogens. The question remains to what extent the course of pancreatitis is influenced by its etiology. Biliary, alcoholic, traumatic and postoperative pancreatitis is usually severe, pancreatitis associated with viroses and induced by drugs is usually mild.
Four hundred and fifty-four consecutive patients who had had their gallbladder removed were interviewed to determine the presence of upper abdominal pain, increased serum alkaline phosphatase and/or serum amylase activity. Patients with unexplained upper abdominal pain and/or enzyme abnormalities were offered endoscopic retrograde cholangiopancreatography (ERCP) and manometric evaluations. Dysfunction of the sphincter of Oddi diagnosed by ERCP manometry may account for the abdominal pain seen in 14% of the patients with postcholecystectomy syndrome. It may rarely be the cause of an elevated serum alkaline phosphatase and/or amylase when abdominal pain is not present. Papillary dysfunction is seen in less than 1% of the patients who have had their gallbladders removed. ERCP manometry is recommended in cholecystectomized patients with unexplained abdominal pain suggesting pancreaticobiliary origin.
In 15 patients with duodenal diverticula close to the papilla of Vater we evaluated the motor activity of the sphincter of Oddi by endoscopic biliary manometry. Both basal pressure and phasic activity were similar to those in nine patients without biliopancreatic disease and in 60 patients with common bile duct stones. The anatomical relationship between the papilla and diverticula did not lead to any change in the motor pattern. If juxtapapillary diverticula are associated with a higher prevalence of biliopancreatic disease, dysfunction of the sphincter of Oddi does not seem to play a pathogenic role.
An obstacle to the outflow from the bile duct not only increases bile duct pressure but also facilitates the formation of primary bile duct stones. The bile duct pressure, an indicator of the balance between bile inflow and outflow, was studied postoperatively under similar conditions in 123 patients, who had been operated on for bile duct stones. Secondary bile duct stones had been present in 86 patients (group CC) and primary stones in 26 (group C), while 11 without sphincter of Oddi function were used as a control group. The basal bile duct pressure was similar in groups CC and C, but significantly lower in the controls. Intraductal injection of saline solution caused a similar increase in bile duct pressure in groups CC and C, but not in the controls. Intravenous administration of secretin and somatostatin increased the bile duct pressure in groups CC and C, while a "normal" response to cholecystokinin, a decrease in bile duct pressure, was observed only in group CC. The "abnormal" response to cholecystokinin found in group C indicates a motor dysfunction of the sphincter of Oddi, which may have been responsible for, or at least contributed to, the formation of recurrent bile duct stones in this group.
Delivery of bile into the duodenum involves a series of complex interrelationships between hepatic secretion of bile and pressure differentials generated within the gallbladder, cystic duct and sphincter of Oddi. Theoretically, functional disorders of bile flow may arise from a disturbance of any one of the above factors. A brief review of our present knowledge of the physiology of bile flow and the spectrum of functional biliary tract disorders will be outlined to help explain possible factors which may be involved in biliary tract dysmotility disturbances. The sphincter of Oddi (SO) mechanism is dedicated to maintaining a low pressure system within the hepatic ducts which allows hepatic secretion to proceed irrespective of bile flow rate. Partial obstruction at the SO segment can give rise to intermittent or persistent upper abdominal pain. We classify sphincter of Oddi (SO) motor dysfunction into two broad categories: 1. SO stenosis: defined as a structural narrowing of part or all of the SO segment, and 2) SO dyskinesia: defined as a primary disorder of SO tonic/phasic motor activity. We have attempted to deal with an overlap in etiology of SO motor dysfunction by developing patient group classifications. Biliary I-patients with biliary-type pain, abnormal liver function tests (SGOT; al PO4 greater than 2 x normal) documented on 2 or more occasions, delayed drainage of ERCP contrast greater than 45 min, and dilated CBD greater than 12 mm diameter; Biliary II-patients with biliary-type pain but only 1 or 2 of the above criteria; Biliary III-patients with only biliary-type pain and no other abnormalities. A few of these patients may have primary SO dyskinesia.
We report a case of post-surgical temporary functional stenosis of the sphincter of Oddi and biliary leak in a patient with a previous Billroth II reconstruction who had undergone cholecystectomy, surgical choledochotomy and sphincterotomy for biliary calculi. The patient was treated by creation of an internal/external biliary drainage using the T-tube access with an unreported technique.
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BACKGROUND: Reflux of pancreatic juice into the biliary tract is a well-known risk factor for the development of biliary carcinoma. In this study, we investigated the significance of bile-reflux into the pancreatic ducts in pancreatic carcinogenesis, especially in the development of carcinoma in the main pancreatic duct in hamsters. MATERIALS AND METHODS: Syrian hamsters were subjected to three different surgical procedures: cholecystoduodenostomy with dissection of the extrahepatic bile duct on the distal end of the common duct (Model A); cholecystoduodenostomy along with a dissection of the common bile duct (Model B); or simple laparotomy (Model C). The animals then received weekly subcutaneous injections of N-nitrosobis(2-oxopropyl)amine (BOP), for 9 weeks, and were killed for pathological investigation at 16 weeks after the initial BOP administration. RESULTS: Pancreas carcinomas developed in 95, 88, and 90% of the Model A hamsters (n = 22), B (n = 24), and C (n = 21), respectively. The induced pancreatic tumors were histologically classified into four types: papillary; tubular; cystic adenocarcinoma; or intraductal carcinoma of the main pancreatic duct consisting of intraductal papillary carcinoma (IPC) and intraductal tubular carcinoma (ITC). The number and the incidence of IPCs induced in Model A hamsters were 24 lesions and 77% and were statistically higher than those in Model B (7 lesions and 29%) and C hamsters (7 lesions and 33%) (P < 0.01). Bile-reflux into the pancreatic ducts was clearly demonstrated in only hamsters of Model A by means of Indocyanine green injection via the portal vein. Proliferative cell nuclear antigen labeling indices of the epithelial cells in the main pancreatic duct in hamsters, with no BOP treatment, were 3.8, 0.8, and 1.1% in Models A (n = 10), B (n = 10), and C (n = 10), respectively, and the difference was statistically significant (P < 0.01). CONCLUSIONS: Our findings suggest that bile-reflux into the pancreatic ducts is a significant factor predisposing to the development of IPC of the pancreas through an acceleration of epithelial cell kinetics of the main pancreatic duct.
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Between 1978 and 1989, 13 of 48 patients with anomalous union of the pancreaticobiliary ductal system (AUPBD) were diagnosed as having acute pancreatitis. We have studied the clinical, radiologic, and surgical features of these 13 patients. A transient rise in the intraductal pressure of the pancreatic duct during an episode of abdominal pain is responsible for pancreatitis in patients with AUPBD. This rise in the intraductal pressure must be due to bile reflux into the pancreatic duct when an abnormally long common channel is blocked by cholelithiasis, protein plug, or dysfunction of the sphincter of Oddi. The pancreatitis resolves when the common channel obstruction is removed, and bile and pancreatic juice flow easily into the duodenum. We believe that this phenomenon is responsible for acute relapsing pancreatitis. It is our belief that the pancreas appears almost normal during symptom-free intervals.
Whole-liver transplantation is an accepted and successful method of treating end-stage liver disease. As a result of the shortage of cadaveric livers, split-liver transplantation and living donor liver transplantation are becoming more commonplace. Ultrasonography (US) is the initial imaging modality of choice for detection and follow-up of early and delayed complications from all types of liver transplantation. Vascular complications include thrombosis and stenosis of the hepatic artery, portal vein, or inferior vena cava, as well as hepatic artery pseudoaneurysms and celiac artery stenosis. Biliary complications include leaks, strictures, stones or sludge, dysfunction of the sphincter of Oddi, and recurrent disease. Neoplastic disease in the transplanted liver may represent recurrent neoplasia or posttransplantation lymphoproliferative disorder. Parenchymal disease may take the form of a focal mass or a diffuse parenchymal abnormality. Perihepatic fluid collections and ascites are common after liver transplantation. Knowledge of the surgical technique of liver transplantation and awareness of the normal US appearance of the transplanted liver permit early detection of complications and prevent misdiagnosis.
OBJECTIVE: Needle-knife sphincterotomy (NKS) is used to achieve biliary access when routine cannulation methods have been unsuccessful. The aim of this study was to analyze the results of NNS in patients with an inaccessible common bile duct (difficult cannulation) using standard techniques in endoscopic retrograde cholangiopancreatography and the factors associated with the success of this procedure and complications. MATERIAL AND METHODS: We performed a prospective study of 72 patients who underwent NKS performed by the same endoscopist (J.E.) because of difficult cannulation of the common bile duct between January 1998 and December 2004. The results were analyzed in terms of successful biliary access, whether this was achieved in one or more sessions, its possible association with the underlying disease, and the incidence and severity of complications. RESULTS: Seventy-two NKS were performed from a total of 1062 sphincterotomies (6.7%). A total of 77.7% of the patients underwent prior implantation of a pancreatic prosthesis (NKS-PP). The final diagnosis was: choledocholithiasis (31.9%), cancer of the pancreas (16.6%), cholangiocarcinoma (13.8%), benign stenosis (8.3%), dysfunction of the sphincter of Oddi (6.9%), normal (6.9%), and miscellaneous (13.8%). Cannulation was successful in 87.5% (63/72), and was achieved in the first session in 73% (46/63). Biliary access was achieved in 72.7% of patients (16/22) with biliopancreatic neoplasms versus 94% (47/50) of those with other diagnoses (p = 0.03). Eleven patients (15.2%) presented 12 complications (16.6%) (6 pancreatitis, 4 cholangitis, 1 papillary hemorrhage, and 1 portal vein filling). The use of a pancreatic prosthesis was related to a higher success rate and significantly fewer complications (p = 0.03). CONCLUSIONS: NKS-PP can be a safe procedure in patients with difficult cannulation of the common bile duct. The presence of biliopancreatic neoplasm is a risk factor for failure to achieve biliary access compared with other diagnoses. The complication rate was similar to that found in other studies. No cases of severe pancreatitis or perforations were found.
It has not been firmly established whether dysfunction of the sphincter of Oddi, biliary dyskinesia, exists as a distinct clinical entity. Improved diagnostic methods, such as ERCP and different manometric studies combined with provocation tests, have provided objective evidence that, in some patients with what is termed the postcholecystectomy syndrome, a spastic sphincter of Oddi is a cause of their complaints. Controlled randomised clinical studies are lacking, but previous results have shown that either operative or endoscopic papillotomy might be indicated in some patients with sphincter Oddi dyskinesia.
AIM: To investigate the therapeutic effect of endoscopic sphincterotomy (EST) in the treatment of choledocholithiasis and stenosing papillitis. METHODS: A total of 1 026 patients undergoing EST during July 1983 to May 2003 at the institute were retrospectively analyzed. Chronic pancreatitis was diagnosed in 63 (6.1%), cholecystolithiasis and choledocholithiasis in 549 (53.5%), stones in residual biliary duct in 249 (24.3%), stenosing papillitis in 228 (22.2%). In patients with simple stenosing papillitis, most incisions were within 0.5-1 cm in length. As for patients with chronic pancreatitis simultaneously, selective pancreatic sphincterotomy was performed, and incision was within 0.5-0.8 cm in length. For stones less than 1 cm, incision was from 1 to 1.5 cm, and for those larger than 1 cm, incision ranged from 1.5 to 3 cm. For stones more than 2 cm in diameter, detritus basket rather than simple incision was chosen. RESULTS: Of the 798 patients with choledocholithiasis, 764 (93.5%) had successful stone clearance, 215 (94.3%) out of 228 cases of stenosing papillitis were cured totally, while 63 had chronic pancreatitis developed from stenosing papillitis, 57 (90.1%) had sound remission of symptoms, though membranous stenosis emerged in 13 of 57 which was treated with balloon dilatation. After the operation, only 21 cases (2.1%) had complications such as severe pancreatitis and incision bleeding. None of the patients died. CONCLUSION: EST is an ideal surgical management with mini-invasion in the treatment of choledocholithiasis and stenosing papillitis.
BACKGROUND: MRCP has replaced ERCP as the diagnostic tool in diseases in the biliary and pancreatic ducts. Secretin increases the secretion to ducts, and this has been reported to improve MRCP image quality. MATERIAL AND METHODS: We report our experience with S-MRCP in our first 20 patients. Secretin was given intravenously and images were obtained every minute for 10 minutes. These images were compared with MRCP images taken before and after secretin stimulation. RESULTS: New information was yielded in 18 cases, i.e. information not observed in previous radiological examinations. INTERPRETATION: In diagnostics of dysfunction of the sphincter of Oddi, the method may be useful, given the functional aspect of the procedure where increased pressure in the ducts may lead to pain. It may further improve the diagnostics of pancreatic cancer versus pancreatitis, in pancreas divisum and sclerosing cholangitis. The method is also valuable for clarifying whether there is injury to the pancreatic duct after blunt abdominal trauma. Surgical common bile duct injuries may be better assessed than with any other method. In difficult pancreatic and biliary investigations, S-MRCP seems to be a useful and complication-free supplement to existing diagnostic methods.
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