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PubMed2001

Effect of somatostatin on the sphincter of Oddi in patients with acute non-biliary pancreatitis.

BACKGROUND: Somatostatin has been used to prevent pancreatitis after endoscopic retrograde cholangiopancreatography but its effect on acute non-biliary pancreatitis is still unclear. AIM: The purpose of this study was to evaluate the function of the sphincter of Oddi (SO) and the effect of somatostatin on patients with non-biliary pancreatitis. METHODS: Twenty patients (18 males, two females) with acute pancreatitis (alcoholic 18, idiopathic two) received SO manometry within one week after admission. After baseline measurement, a bolus dose of somatostatin (Stilamin, Serono) 250 microg was infused slowly, and SO manometry was repeated after five minutes. Continuous infusion of somatostatin 250 microg/h was given for 12 hours after SO manometry. Serum amylase, lipase, glucose, and C reactive protein (CRP) levels were examined before and after somatostatin infusion. RESULTS: SO manometry was unsuccessful in six patients due to contracted sphincter. In the remaining 14 patients, high SO basal pressure (SOBP >40 mm Hg) was found in seven patients. After somatostatin infusion, mean SOBP decreased from 48.8 (29) to 31.9 (22) mm Hg (p<0.01). One patient had a paradoxical reaction to somatostatin (SOBP increased from 30 to 50 mm Hg) while the other 13 patients had a fall in SOBP after somatostatin. One patient developed abdominal pain with a serum amylase level of 2516 IU/l after SO manometry. No other side effects or changes in amylase, lipase, glucose, or CRP levels were observed in the other 19 patients after SO manometry and somatostatin infusion. DISCUSSION: Sphincter of Oddi dysfunction is common in patients with acute non-biliary pancreatitis and in most cases somatostatin can relax the sphincter.

Acute Disease↗

PubMed1995

Abnormal sphincter of Oddi response to cholecystokinin in postcholecystectomy syndrome patients with irritable bowel syndrome. The irritable sphincter.

Standard biliary manometry, including cholecystokinin (CCK) provocation, was performed on 42 consecutive patients (36 F, 6 M, median age 45 years) with postcholecystectomy syndrome (PCS) who had no evidence of organic disease but who had objective clinical features suggesting sphincter of Oddi dysfunction (SOD) (classes I and II). Patients were subdivided into those with (N = 14) and without (N = 28) irritable bowel syndrome (IBS) using a validated symptom questionnaire based on the modified Rome criteria. Resting sphincter of Oddi (SO) motor parameters (basal pressure, contractile amplitude and frequency, and proportion of retrograde contractions), the presence of abnormal manometry, and the presence of an abnormal response to CCK were compared in the two groups. No significant differences in resting parameters of SO motor activity between patients with and without IBS were observed, and abnormal biliary manometry as a whole was not more prevalent in either group (8/13 and 18/27, respectively). An abnormal response to CCK (failure of complete inhibition of phasic contractions), however, was demonstrated in five of 12 patients with IBS compared with only one of 23 patients without IBS (P = 0.01). In patients with postcholecystectomy SOD, an abnormal response of the SO to CCK thus appears to be an important feature of the subset of patients with concomitant IBS.

Biliary Dyskinesia↗

PubMedDate not supplied

The influence of sphincterotomy and hepatic plexus vagotomy on ascending infections of the biliary tract: an experimental study in dogs.

BACKGROUND/AIMS: Hypertonic dyskinesia of the sphincter of Oddi is an important factor in the pathogenesis of postcholecystectomy syndrome, and this condition is usually treated by endoscopic sphincterotomy. However, it has been demonstrated that the biliary tract may also be contaminated after sphincterotomy. In various experimental studies, it has been established that the choledochal pressure decreases by a mean of 32% to 28% after hepatic plexus vagotomy. This experimental study was performed to investigate whether hepatic plexus vagotomy and/or sphincterotomy result in contamination of the biliary tract. METHODOLOGY: Thirty street dogs were divided into three equal groups. The three groups underwent simple laparotomy, transduodenal papillotomy, hepatic plexus vagotomy, respectively, and gallbladder bile samples were taken from all of them. Relaparotomy was performed after four weeks, and again, bile samples were taken from the gallbladder. All bile samples were examined microbiologically. RESULTS: Bacteria were not found in the first bile samples taken from the three groups. Bacteria were not found in the bile samples taken during the second surgery in the simple laparotomy and hepatic plexus vagotomy groups. However, both aerobic and anaerobic bacteria were found in the papillotomy group in seven of the ten dogs. CONCLUSION: These results demonstrate that hepatic plexus vagotomy decreased choledochal pressure and did not cause contamination of the biliary tract. It may be a treatment of choice to prevent postcholecystectomy syndrome resulting from sphincter of Oddi dysfunction.

Animals↗

PubMed1991

Distension of the gall bladder inhibits sphincter of Oddi motility in humans.

Studies in animals have suggested a neural reflex between the gall bladder and the sphincter of Oddi. The aim of this study was to investigate whether sphincter of Oddi motility is altered by distension of the gall bladder in humans. Sphincter of Oddi motility was recorded intraoperatively in 10 patients undergoing elective cholecystectomy for gall stones. The manometry was performed by a triple lumen constantly perfused catheter which was introduced through the cystic duct and positioned across the sphincter of Oddi to record sphincter basal pressure, wave amplitude, and frequency of contractions. In five patients a separate catheter was introduced into the gall bladder after ligation of the cystic duct. This catheter was used to distend the gall bladder. Sphincter of Oddi pressures were measured before, during, and after the distension. In a separate control group of patients (n = 5) basal sphincter of Oddi activity was recorded without distension of the gall bladder. Distension of the gall bladder decreased sphincter of Oddi basal pressure from (mean (SD] 22.8 (8.5) mmHg to 18.6 (6.5) mmHg (p = 0.01, paired t test) and frequency of sphincter of Oddi contractions decreased from 2.6 (1.6) to 1.1 (1.3) contractions/min (p = 0.003, paired t test). The results were significantly different from those of the control group (p less than 0.05, unpaired t test) during the same time period (four minutes). Pulse rate and blood pressure were not affected by the gall bladder distension. The results suggest a local reflex between the gall bladder and the sphincter of Oddi that might be important in the regulation of the pressure within the bile ducts and flow across the sphincter. This reflex is likely to be neurally mediated and injuries to it may be important in the aetiology of postcholecystectomy sphincter of Oddi dysfunction.

Adult↗

PubMed1996

Effect of octreotide on sphincter of Oddi motility in patients with acute recurrent pancreatitis: a manometric study.

Sphincter of Oddi dysfunction has been reported as a cause of acute idiopathic recurrent pancreatitis (IRP). Octreotide, a long-acting somatostatin analogue, is an antisecretory drug used in the treatment and prevention of acute pancreatitis. Its action on sphincter of Oddi motility is controversial and no data are available for IRP patients. The aim of this study was to assess sphincter of Oddi motor response to acute administration of octreotide in patients with past attacks of acute pancreatitis without identification of any evident aetiological factor. Six patients (four male, two female; mean age +/-SD, 38.8+/-9 years) suffering from acute pancreatitis for at least 3 months before the examination were submitted to sphincter of Oddi manometry. After a basal recording lasting at least 2 min, octreotide, 0.05 mg i.v., was administered and the recording repeated. Intraduodenal pressure was taken as the zero reference and the basal sphincter of Oddi pressure and amplitude and frequency of phasic contractions were calculated before and after octreotide administration. No significant pre- vs post-octreotide differences were observed in basal pressure (41.9+/-24 vs 47.5+/-33 mm Hg, respectively) or in amplitude of phasic contractions (164.6+/-33 vs 170.8+/-18 mm Hg). With a latency of about 1 min, octreotide administration caused a high-frequency phasic activity in all cases (mean frequency, 5.5+/-2.2 contractions/min before and 9.8+/-2 after octreotide; P < 0.04). After the procedure acute pancreatitis (prolonged abdominal pain and serum amylase levels more than three-fold the normal values) developed in five patients. In conclusion, our data suggest that acute administration of octreotide may induce tachyoddia and thus a rise in sphincter of Oddi pressure, with possible impairment of biliary-pancreatic outflow.

Acute Disease↗

PubMed2002

Relative effects of dihydropyridine L-type calcium channel antagonism on biliary, duodenal, and vascular tissues: an in vivo and in vitro analysis in Australian brush-tailed possum.

Nifedipine is used to treat sphincter of Oddi dysfunction. Its effects on the biliary system and duodenum in relation to its known vascular actions are unclear. Our aims were to determine the relative tissue sensitivities to dihydropyridine L-type calcium channel antagonism in the sphincter of Oddi, gallbladder, duodenum, and vasculature. For in vivo studies, 23 possums received nifedipine at three different doses with blood pressure and sphincter of Oddi manometry recordings. For in vitro studies, tissues from 28 possums were pretreated with nicardipine (10(-8)-10(-5) M) and cumulative concentrations of agonist were administered (carbachol, norepinephrine at 10(-9)-10(-5) M). In in vivo studies, blood pressure fell significantly at a lower dose than sphincter of Oddi motility. In in vitro studies, the sphincter of Oddi was more sensitive than arterial tissue, with the duodenum especially sensitive. In conclusion, in the possum we found that L-type channel antagonism in vivo was more potent to the vasculature than the sphincter of Oddi but this was not confirmed in vitro.

Animals↗

PubMed2005

The role of endoscopic retrograde cholangiopancreatography and endoscopic ultrasound in diagnosis and treatment of acute pancreatitis.

Endoscopic retrograde cholangiopancreatography (ERCP) is an important tool for diagnosis and therapy in acute and recurrent pancreatitis. While treatment of biliary disorders leading to pancreatitis is common practice, over the past several years many specialized centers have been directing traditional biliary techniques such as sphincterotomy and stenting towards the pancreas. A justifiable fear of pancreatitis and other complications has caused many endoscopists to shy away from pancreatic endotherapy, but refinements in technique, extensive experience, and most notably the routine use of pancreatic stenting to prevent post-ERCP pancreatitis has opened up the field and allowed for endoscopists in specialized centers around the world to perform diagnostic and therapeutic ERCP of the pancreas safely and effectively. In acute gallstone pancreatitis, the benefit of therapeutic ERCP including biliary sphincterotomy has been proven in randomized controlled trials. There are also data to support the role of ERCP directed at the pancreatic sphincters and ducts in treatment of acute relapsing pancreatitis due to pancreas divisum, sphincter of Oddi dysfunction, smoldering pancreatitis, pancreatic ductal disruptions, and perhaps even in evolving pancreatic necrosis. Many causes of apparently idiopathic pancreatitis can be discovered after an extensive evaluation with endoscopic ultrasound (EUS), magnetic resonance cholangiopancreatography (MRCP) and ERCP with sphincter of Oddi manometry. ERCP often allows treatment of the underlying cause. Because of the inherent risks associated with ERCP, particularly when directed toward the pancreas, the role of ERCP in acute and especially recurrent pancreatitis should be primarily therapeutic with attempts to establish diagnosis whenever possible by less risky techniques including EUS and MRCP. With the added techniques, devices, skill-sets, and experience required, pancreatic endotherapy should preferably be performed in high volume tertiary referral settings. ERCP for diagnosis and treatment of severe or acute relapsing pancreatitis is also best performed using a multidisciplinary approach involving endoscopy, hepatobiliary-pancreatic surgery, and interventional radiology.

Acute Disease↗

PubMed1988

Sphincter of Oddi manometry: comparison of microtransducer and perfusion methods.

There are two approaches to endoscopic sphincter of Oddi manometry, the microtransducer method and the perfusion method. Data reported by us and others are reviewed, with the aim of comparing the two techniques. Biliary pressure, pancreatic duct pressure, and sphincter of Oddi phasic wave activity can be measured by both of these methods. Easy handling and the capability of recording the mode of phasic wave propagation with a multilumen catheter are present advantages of perfusion manometry over the microtransducer method. Because there is no need for perfusion of fluid, the equipment needed for microtransducer manometry is simpler than that needed for the perfusion method, and the microtransducer technique may be more suitable for prolonged recording. An inter-study comparison of manometric data is easier with microtransducer manometry, but must await the collection of more data. Manometric differences between various diseases are still inconsistent, whereas there is no question of the effect of sphincterotomy on pressure values, with the exception of pancreatic duct and sphincter pressures. The possibilities of diagnosing sphincter of Oddi dysfunction, and of predicting the response to sphincterotomy have been received with enthusiasm. However, whether the findings obtained by endoscopic manometry over relatively short periods of time can be considered representative of overall sphincter function is now being questioned since the presence of physiologic cyclic changes in sphincter of Oddi phasic activity in phase with the migrating motor complex of the duodenum was demonstrated. Hormonal or pharmacological stimulation of sphincter activity may help us overcome this problem.

Ampulla of Vater↗

PubMed2003

Acute idiopathic pancreatitis: does it really exist or is it a myth?

BACKGROUND: Acute pancreatitis is a severe disease with considerable morbidity and mortality. Gallstones and alcohol abuse are the most frequent causes (75% of patients). Other well-known causes are: hyperlipidemia, hypercalcaemia, abdominal surgery and drugs. In 10%-40% of patients however, no cause is identified after initial diagnostic evaluation: acute idiopathic pancreatitis. Identifying a cause in these patients is important, since the recurrence rate is high. METHODS: A systematic review of the current literature was performed to identify possible causes, diagnoses and treatment options of acute idiopathic pancreatitis. Relevant literature was found via Pubmed. RESULTS: The presence of microlithiasis or biliary sludge is an important cause of acute 'idiopathic' pancreatitis (up to 80% of patients). Microlithiasis and sludge can be detected by transabdominal/endoscopic ultrasonography, ERCP or polarizing light microscopy of bile. Cholecystectomy is the treatment of choice, whereas endoscopic sphincterotomy and ursodeoxycholic acid maintenance therapy are effective alternatives. Sphincter of Oddi dysfunction can be identified as the cause of acute 'idiopathic' pancreatitis in up to 30% of patients. Manometry of Oddi's sphincter is the gold standard for its diagnosis. Endoscopic sphincterotomy prevents recurrence in most patients. Anatomic abnormalities such as major papilla stenosis, pancreas divisum, pancreatic duct strictures and tumours may also cause acute 'idiopathic' pancreatitis. Endoscopic sphincterotomy and surgery are effective treatments. Finally, genetic screening may reveal gene mutations as the cause of acute 'idiopathic' pancreatitis. CONCLUSIONS: Acute 'idiopathic' pancreatitis is a severe disease with a high recurrence rate. Extensive diagnostic investigations may lead to a cause in >90% of patients.

Acute Disease↗

PubMed2004

[Evaluation of endoscopic sphincter of Oddi manometry in patients with biliopancreatic diseases].

Diagnostic ability of endoscopic sphincter of oddi manometry for 112 patients with biliopancreatic diseases (including 12 patients of normal) was evaluated. The presence of abnormal high pressure was recognized in 50% of suspected sphincter of oddi dysfunction (SOD). 56% of cholecystolithiasis, 67% of cholecystocholedocholithiasis and 50% of pancreatic stones. Many patients with abdominal pain of suspected SOD or stones of biliopancreatic ducts were considered to have possibility of the complication of papillary stenosis. It was thought that endoscopic sphincter of oddi manometry was a useful method of confirming the presence of SOD.

Calculi↗

PubMed1990

Idiopathic acute pancreatitis.

In most patients presenting with acute pancreatitis, the cause can be established on the basis of initial history, physical examination, laboratory studies, and abdominal sonography. Patients with unexplained pancreatitis at that point are often considered to have idiopathic disease. However, a cause and, often, effective treatment to prevent recurrent pancreatitis are possible in many of these patients if an aggressive diagnostic approach is taken to discover undiagnosed hyperlipidemia, occult gallstones, abnormalities of the bile and pancreatic ducts, sphincter of Oddi dysfunction, pancreatic cancer and other tumors, and cystic fibrosis (in children and young adults).

Acute Disease↗

PubMed2005

Is sphincter of Oddi manometry a risk factor for pancreatitis? A different view.

Studies suggest a causal relationship between sphincter of Oddi manometry (SOM) and acute pancreatitis, presumably due to water instillation in the ductal system. In this article, critical analysis of the existing studies attributes the high risk of acute pancreatitis with SOM to "association due to confounding" rather than to "causation." This conclusion is based on two pieces of evidence: The first is lack of biologic plausibility: Biologic evidence is lacking to support the hypothesis that water instillation during SOM can induce acute pancreatitis. The second is confounding evidence: Manometric studies show considerable variation in the risk of post-procedure pancreatitis (4% to 30%), which suggests that other important factors besides SOM influence the adverse outcome. These studies did not control for other variables, which are well known to predispose to pancreatitis and therefore may act as confounding factors. Two studies that assessed the independent role of SOM in causation of acute pancreatitis showed that SOM is not an independent predictor of acute pancreatitis. It is the underlying disorder sphincter of Oddi dysfunction, and not the "SOM" procedure, that predisposes patients to post-procedure acute pancreatitis.

Acute Disease↗

PubMed2003

Motility and dysmotility of the biliary tract.

Muscle fibers in the biliary tree, and therefore the potential for dysmotility, are located in the gallbladder and the sphincter of Oddi. Dysmotility at either site is a potential cause of biliary pain in the absence of stones, although significant controversy persists. Diminished gallbladder emptying measured by biliary scintigraphy is an indication for cholecystectomy, although studies are contradictory regarding clinical benefit. It is likely that careful selection of patients for cholescintigraphic testing, many of whom have had missed stones or sludge, will identify patients who benefit from cholecystectomy. However, given the increased incidence of gallbladder stasis in functional gastrointestinal disorders, wide use of this study in patients with abdominal symptoms leads to a frequent failure to respond to cholecystectomy. Sphincter of Oddi dysfunction (SOD) has been best studied in patients with biliary type pain who have had prior cholecystectomy. Much less understood is the association of SOD with idiopathic recurrent acute pancreatitis and chronic pancreatitis. The least-studied clinical association for SOD is in patients with biliary pain and intact gallbladders. Elevated basal sphincter of Oddi pressure is predictive of clinical response to sphincterotomy in patients with postcholecystectomy pain in two randomized sham-controlled studies. However, patients with suspected SOD have the highest complication rate from endoscopic retrograde cholangiogram and sphincterotomy, and, therefore, careful patient selection is mandatory.

Adult↗

PubMed1995

Success and yield of second attempt ERCP.

Endoscopic retrograde cholangiopancreatography (ERCP) has been shown to be an accurate and reliable method to evaluate biliary and pancreatic disorders. When an attempt to perform ERCP fails, the managing physician must decide whether to repeat the procedure or rely on other alternatives. We tallied the data from 113 patients referred to our institution for repeat ERCP after a failed attempt at another hospital. This group represented approximately 5% of the total population studied during that period of time. All of the patients had undergone one or more unsuccessful ERCP(s) and were referred to our center for another attempt at ERCP. Using a variety of techniques, we were successful in cannulating the desired duct in 96% of attempts. Pathologic findings were present in 64% of cases, of which 22% were sphincter of Oddi dysfunction. Thus, second attempt ERCP is generally worthwhile if clinically indicated and ERCP expertise is geographically available.

Cholangiopancreatography, Endoscopic Retrograde↗

PubMed2002

Octreotide relaxes the hypertensive sphincter of Oddi: pathophysiological and therapeutic implications.

OBJECTIVES: As our understanding of the pathophysiology of sphincter of Oddi dysfunction (SOD) expands, new avenues arise for pharmacological intervention. Recent evidence suggests that SOD results from a loss of myenteric plexus inhibitory neurons resulting in unopposed cholinergic tone. Octreotide inhibits postganglionic cholinergic neurons, and thus we hypothesize that administration of octreotide will decrease sphincteric pressure in individuals with SOD. METHODS: Thirty-eight patients presenting with recurrent abdominal pain and SOD (basal pressure > 40 mm Hg) were studied. The study was prospective, placebo controlled, and blinded. Patient allocation was consecutive. Sphincter of Oddi manometry was performed in standard fashion. The test group (n = 19) received octreotide acetate (100 microg i.v.), and the control group (n = 19) received i.v. saline. Basal, phasic, and duct pressures as well as phasic amplitude and frequency were recorded before and 3 min after the i.v. infusion. Changes in these parameters before and after i.v. infusions were compared. RESULTS: Octreotide caused a statistically significant reduction in peak and basal sphincter of Oddi pressures relative to saline (p < 0.01 and p < 0.001). Octreotide did not significantly affect wave amplitude, wave frequency, or duct pressure. CONCLUSIONS: Octreotide has the potential to be a valuable addition to the armamentarium for the medical management of SOD.

Adult↗

PubMed2006

Role of endoscopic evaluation in idiopathic pancreatitis: a systematic review.

In approximately 20% of patients with acute pancreatitis, a cause is not established by history, physical examination, routine laboratory testing, and abdominal imaging. For those with a single unexplained attack, the role of invasive evaluation with endoscopic retrograde cholangiopancreatography is unsettled but has been generally limited to those patients with suspected bile duct stones or malignancy. Recent studies suggest that microlithiasis is causative in up to 75% of patients with an unexplained attack and gallbladder in situ, whereas sphincter of Oddi dysfunction is most prevalent in those with recurrent attacks who have previously undergone cholecystectomy. EUS has been shown to be highly accurate for the identification of gallbladder sludge, common bile duct stones, and pancreatic diseases. Given this apparent diagnostic utility, an EUS-based strategy may be a reasonable approach to evaluate patients with a single idiopathic attack. ERCP and sphincter of Oddi manometry should generally be reserved for patients with multiple unexplained attacks and negative EUS results, especially for those patients who have previously undergone cholecystectomy.

Bile↗

PubMed1986

Effect of analgesic drugs on the electromyographic activity of the gastrointestinal tract and sphincter of Oddi and on biliary pressure.

Continuous biliary pressure and electromyographic activity of the sphincter of Oddi and gastrointestinal tract were recorded in conscious opossums following administration of analgesic drugs. Morphine, meperidine, and pentazocin increased significantly the duration of the migrating motor complex (MMC) cycle. Periods of 1-2 minutes of intense burst of spike potentials were seen in the sphincter of Oddi and duodenum following administration of morphine (8 experiments), meperidine (6 experiments), and pentazocin (3 experiments). The biliary pressure in the control studies was similar to that following administration of all analgesics in the animals with gallbladder and following instillation of tramadol, metamizol, and acetylsalicylic acid in animals with no gallbladder. However, the biliary pressure was significantly higher following administration of morphine, meperidine, and pentazocin in the animals with no gallbladder. It is concluded from this study that morphine, meperidine, and pentazocin may cause important disturbances in the motility of the sphincter of Oddi and gastrointestinal tract. These myoelectric disturbances may cause an increase in the biliary pressure in animals that have been subjected to cholecystectomy, but not in animals with intact gallbladder. The gallbladder may accommodate the bile produced by the liver during periods of sphincter of Oddi dysfunction and thus impede an increase in the biliary pressure.

Ampulla of Vater↗

PubMed2002

Evidence-based approach to idiopathic pancreatitis.

The causes of recurrent acute pancreatitis, including the newly recognized genetic causes, are reviewed. The pitfalls of overcalling the diagnosis of pancreatitis in patients with abdominal pain or other symptoms and the role of a careful history are emphasized. The presence of undetectable microlithiasis in patients with unexplained pancreatitis is discussed. The popular notion of pancreas divisum and sphincter of Oddi dysfunction as causes of pancreatitis is challenged, as is the role of endotherapy in these conditions.

Acute Disease↗