Certain aspects of normal and abnormal motility of sphincter of Oddi

Applications of electromyographic and endoscopic manometric techniques in experimental and clinical studies have enhanced our knowledge of the normal physiology and motility disturbances of the sphincter of Oddi. The sphincter of Oddi has an active role in coordinating the time and rate of secretion of biliopancreatic juice into the duodenum. In the opossum, the sphincter of Oddi exhibits spontaneous contractions that migrate distally along the sphincter and expels its contents into the duodenum. Although the motor activity of the sphincter of Oddi is independent from that of the duodenum, there is a correlation between the frequency of bursts of spike potentials in the sphincter of Oddi and the migrating motor complex phases in the duodenum. Abnormal motility of the sphincter of Oddi has been reported during endoscopic manometric evaluation of patients with choledocholithiasis and sphincter of Oddi dyskinesia. Patients with common bile duct stones have an increase in the frequency of retrograde propagation of phasic waves. Elevation of basal pressure as well as an increase in the frequency and amplitude of sphincter of Oddi phasic waves and the common bile duct-duodenum gradient pressure may occur in patients with sphincter of Oddi dyskinesia. Endoscopic manometric studies of the sphincter of Oddi may become an important method to diagnose sphincter of Oddi dyskinesia.     

Sphincter of Oddi motor activity in patients with stones in gall-bladder, common bile duct or intrahepatic duct and the effect of morphine

Abstract Sphincter of Oddi phasic motor activity and common bile duct pressure were investigated in controls (seven patients) and in patients with gall-bladder stones (five patients), common bile duct stones (15 patients), or intrahepatic stones (13 patients). There were no significant differences in amplitude and frequency of the phasic activity or the common bile duct pressure between the controls and disease groups. Basal pressure of the phasic contraction, however, was significantly lower in patients with common bile duct or intrahepatic stones than in the controls or gall-bladder stone group. The administration of morphine, known to cause spasm of the sphincter of Oddi, increased the basal pressure and frequency of the phasic waves in all groups, while the amplitude remained unchanged. Response to morphine in patients with common bile duct or intrahepatic stones was similar to the controls. However, the basal pressure in these latter groups was lower than in the controls, even after stimulation by morphine. The high incidence of bacterial growth in bile from these patients hitherto reported may be attributable to ascending infection possibly resulting from the low basal pressure of the sphincter of Oddi.     

Biliary tract motor dysfunction

Gallbladder and sphincter of Oddi motility regulates the flow of bile from the liver to the duodenum. During the interdigestive period most secreted bile is diverted into the gallbladder where it is concentrated, but a significant minority of the biliary secretion passes directly into the duodenum. Regulation of this flow is mainly via the phasic contractions of the sphincter of Oddi and the sphincter basal tone. The phasic contractions expel small volumes of fluid into the duodenum, but most of the flow occurs between the contractions and is therefore not dependent on peristaltic pumping, but rather on a small pressure gradient. During fasting, just prior to duodenal phase III activity, the gallbladder expels up to 40% of its volume and the sphincter phasic contractions increase. Following a meal, the gallbladder empties its contents, and the sphincter of Oddi resistance is reduced via a fall in basal pressure and inhibition of the amplitude of phasic contractions. Control of this activity is via an interplay of both neuronal and hormonal factors which together have an effect on both gallbladder and sphincter of Oddi motility. Abnormalities in motility are recognized for both the gallbladder and the sphincter of Oddi. Gallbladder dyskinesia is objectively diagnosed using the radionuclide GBEF. In patients with a GBEF less than 40% cholecystectomy results in relief of symptoms. In postcholecystectomy patients sphincter of Oddi dysfunction presents as either biliary-like pain or idiopathic recurrent pancreatitis. Endoscopic sphincter of Oddi manometry provides the most objective diagnostic information. In patients with a sphincter of Oddi stenosis, characterized manometrically as an elevated basal pressure, division of the sphincter results in relief of symptoms. For patients with biliary-like pain, division is performed as an endoscopic sphincterotomy, whereas for patients with idiopathic recurrent pancreatitis, a sphincteroplasty and pancreatic duct septectomy are required.     

Sphincter of Oddi: Function, dysfunction, and its management

The most common functional disorder of the biliary tract and pancreas relates to the activity of the Sphincter of Oddi. The Sphincter of Oddi is a small smooth muscle sphincter strategically placed at the junction of the bile duct, pancreatic duct, and duodenum. The sphincter controls flow of bile and pancreatic juices into the duodenum and prevents reflux of duodenal content into the ducts. Disorder in its motility is called Sphincter of Oddi dysfunction. Clinically this presents either with recurrent abdominal biliary type pain or episodes of recurrent pancreatitis. Manometry may identify the motility abnormalities, the most clinically significant being an abnormally elevated basal pressure. The most effective treatment once an abnormal basal pressure is identified is division of the sphincter. This is associated with good long-term results.     

Motor Pattern of the Sphincter of Oddi in Patients with Bilioenteric Shunt: A Manometric Study

An endoscopic biliary manometry was performed on 11 patients with a surgical bilioenteric shunt--choledochoduodenostomy--and no pressure gradient between common bile duct and duodenum. Basal pressure and frequency of the phasic waves of the sphincter of Oddi were significantly higher in these patients than in controls or in patients with retained common bile duct stones. These results suggest a functional adaptation of the sphincter of Oddi in an attempt to recover the normal pressure in the biliary tract.     

The sphincter of Oddi and acute pancreatitis--revisited

BackgroundOne of the rare causes of recurrent acute pancreatitis is sphincter of Oddi dysfunction. This condition is objectively diagnosed by manometry of the sphincter of Oddi. An abnormally elevated sphincter of Oddi basal pressure has been shown to predict patients who have a successful outcome after transduodenal sphincteroplasty and pancreatic duct septoplasty.MethodsForty-nine patients presenting with recurrent pancreatitis and who had manometric stenosis of the sphincter of Oddi were treated by transduodenal division of the sphincter of Oddi. Clinical follow-up was conducted over a minimum of 2 years.ResultsIn all, 43 patients were either cured or improved. None of these patients had any further episodes of pancreatitis. Three of these patients developed recurrent symptoms and were noted to have restenosis of the sphincter of Oddi. They were treated by insertion of an endoscopic stent into the pancreatic duct.ConclusionThe results from this series of patients re-affirm the efficacy of transduodenal sphincteroplasty and septoplasty for treatment of sphincter of Oddi stenosis in patients presenting with recurrent acute pancreatitis.     

Endoscopic biliary manometry in patients with suspected sphincter of Oddi dysfunction and in patients with cystic dilatation of the bile ducts

We studied the motility of the sphincter of Oddi in 12 patients with suspected sphincter of Oddi dysfunction, in four patients with cystic dilatation of the bile ducts (two Caroli's cases and two fusiform choledochal cyst cases), and in 33 patients with retained common duct stones. In these last 33 patients, the motor activity of the sphincter of Oddi was similar to that recorded in nine control subjects without pancreatic or biliary diseases. In the suspected Oddi dysfunction cases, both the basal sphincteric pressure and the frequency of the phasic contractions were significantly elevated (P<0.001). Patients with biliary cystic dilatation showed an increased basal pressure, but the frequency of the contractions was elevated in only those with choledochal cysts and the amplitude in only one of the two patients with Caroli's disease. Motor disorders of the sphincter of Oddi provide a basis for an alternative etiopathogenesis of cystic disease of the biliary system and a possible explanation for pain and dilatation of the bile duct in patients with suspected sphincter of Oddi dysfunction.     

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.     

Manometric study of the sphincter of Oddi in patients with and without common bile duct stones

Motor activity of the sphincter of Oddi has been evaluated in 34 patients who underwent ERCP examination. Manometric recordings from the common bile duct and the sphincter of Oddi were performed with a polyethylene triple lumen catheter. At ERCP 16 patients had undamaged biliary ducts; six had undergone cholecystectomy and six had gall bladder stones; 18 patients had common bile duct stones; nine of whom had undergone cholecystectomy, and seven had gall bladder stones. Length and amplitude of the resting sphincter pressure as well as frequency, duration, amplitude, and propagating pattern of phasic contractions did not significantly differ in patients with and without common bile duct stones. Sphincter of Oddi motor activity did not appear to be influenced by the variation in the diameter of the common bile duct or by previous cholecystectomy.     

生长抑素对Oddi括约肌功能的影响

为证实生长抑素对Ｏｄｄｉ括约肌功能的作用，用逆行胰胆管造影下Ｏｄｄｉ括约肌测压研究了生长抑素对２０例患者Ｏｄｄｉ括约肌运动功能的影响。２０例患者中胆总管结石６例，胆总管轻度扩张３例，肝门癌３例，未见明显异常者８例。用低顺应性水灌注系统，三通道测压导管，分别于用药前及静注生长抑素２５０μｇ１分钟后进行Ｏｄｄｉ括约肌测压，以观察Ｏｄｄｉ括约肌的基础压、收缩频率、收缩幅度、收缩间期、传播方式和胆管内压变化。结果显示：用药后Ｏｄｄｉ括约肌基础压降低、收缩频率减慢，其余指标无明显变化。我们认为：生长抑素对Ｏｄｄｉ括约肌有抑制性作用，有利于胆汁和胰液的排出。     

Sphincter of Oddi dysfunction in children with recurrent pancreatitis and anomalous pancreaticobiliary union: an etiologic concept.

BACKGROUND: The exact cause of recurrent pancreatitis among patients with anomalous pancreaticobiliary union is not known. Sphincter of Oddi dysfunction has been implicated as a mechanism. This study evaluated sphincter of Oddi function in children with anomalous pancreaticobiliary union and recurrent pancreatitis and assessed the results of endoscopic sphincterotomy in the management of this condition. METHODS: We retrospectively reviewed 128 endoscopic retrograde cholangiopancreatographic (ERCP) studies performed on children older than 1 year and adolescents with pancreaticobiliary disease. In 64 instances, ERCP was performed because of recurrent pancreatitis. Nine patients underwent sphincter of Oddi manometry followed by endoscopic sphincterotomy, and these patients were included in this study. A basal pressure greater than 35 mm Hg was considered diagnostic for sphincter of Oddi dysfunction. Follow-up data were obtained retrospectively from the patients' relatives and referring physicians. RESULTS: An anomalous pancreaticobiliary union was found in 18 of 64 (28%) patients with recurrent pancreatitis. The 9 patients who underwent sphincter manometry and endoscopic sphincterotomy were 5 girls and 4 boys 2.9 to 17 years of age (mean 7.8 years). A choledochal cyst was found in 7 of these 9 patients. Two patients had anomalous pancreaticobiliary union without common bile duct dilatation. All 9 patients had sphincter of Oddi dysfunction (mean basal pressure 96 +/- 37.8 mm Hg, range 48 to 156 mm Hg). The length of the common channel was 22.8 +/- 5.5 mm, and the length of the sphincter of Oddi segment was 12.1 +/- 1.9 mm (p < 0.001). In all patients the sphincter of Oddi segment was located within the duodenal wall. The mean follow-up period after endoscopic sphincterotomy was 26.4 months (range 18 to 38 months). Eight patients had excellent results defined as absence of symptoms and no subsequent episodes of acute pancreatitis. Treatment of 1 patient was considered moderately successful because the patient still had occasional pain without pancreatic enzyme elevation but no subsequent episodes of acute pancreatitis. One patient had mild postprocedural pancreatitis. CONCLUSIONS: Recurrent pancreatitis and anomalous pancreaticobiliary union are associated with sphincter of Oddi dysfunction in children and adolescents. Endoscopic sphincterotomy is beneficial to these patients.     

Endoscopic sphincterotomy: follow-up evaluation of effects on the sphincter of Oddi

Endoscopic sphincterotomy (ES) alters the structure and motor function of the sphincter of Oddi (SO). The magnitude and duration of these changes, however, have not been critically examined. Before ES, 22 patients with common bile duct stones were evaluated by endoscopic retrograde cholangiography. The pressure gradient between the common bile duct and the duodenum, the SO basal pressure, and the SO peak phasic pressures were obtained. After ES, the electrosurgical incision length was determined using the extended papillotome and an inflated Fogarty balloon as reference. A high correlation existed between the endoscopist's estimate of ES incision size using this technique and the actual length of simulated incisions fashioned in cardboard mounts. These studies were repeated in all 22 patients at 1-yr follow-up and in 8 of these patients at 2-yr follow-up. At 12 mo and 24 mo after ES, the common bile duct (CBD) to duodenal pressure gradient and the sphincter of Oddi basal pressure were virtually eliminated. The amplitude of SO phasic contractions was significantly diminished 12 mo after ES (124 +/- 16 mmHg to 37 +/- 10 mmHg; p less than 0.001), but 24 mo after ES, SO phasic contraction amplitude was not significantly different from the values before ES. Incision length at 1-yr follow-up was reduced in the group of 22 patients from 11.6 +/- 0.8 mm to 8.3 +/- 0.5 mm (p less than 0.001), and in the group of 8 patients from 11.0 +/- 1.5 mm to 7.5 +/- 0.7 mm (p less than 0.025). After an additional 12 mo, however, i.e., 24 mo after ES, the incision length was 6.5 +/- 0.7 mm. There was no significant difference in incision length between the 12-mo and 24-mo examinations. We conclude that after ES, incision length decreases during the first year. There appears to be no further significant reduction in incision length at 2 yr. In addition, the reduction of the CBD to duodenal pressure gradient and the SO basal pressure remain unchanged for at least 2 yr. These manometric findings support the observation that after ES the enlarged opening of the CBD into the duodenum remains open for at least 2 yr.     

Endoscopic pancreatic and biliary manometry in pancreatic, biliary, and papillary disease, and after endoscopic sphincterotomy and surgical sphincteroplasty.

Endoscopic manometry was used to measure pancreatic duct, common bile duct, pancreatic duct sphincter and bile duct sphincter pressures in 43 healthy volunteers and 162 patients with a variety of papillary, pancreatic and biliary disorders. Common bile duct pressure was significantly raised after cholecystectomy, with common bile duct stones and papillary stenosis but pancreatic duct pressure only in papillary stenosis. After endoscopic sphincterotomy mean common bile duct pressure fell from 11.2 to 1.1 mmHg and pancreatic duct pressure from 18.0 to 11.2 mmHg. Distinct pancreatic duct sphincter and bile duct sphincter zones were identified as phasic pressures of 3-12 waves/minute on pull-through from pancreatic duct and common bile duct to duodenum. Pancreatic duct sphincter pressures were higher with common bile duct stones and stenosis whereas bile duct sphincter pressures were higher in pancreatitis and stenosis. Bile duct sphincter activity was present in 60% of patients after surgical sphincteroplasty but 21% of patients after endoscopic sphincterotomy. Endoscopic manometry facilitated the diagnosis of papillary stenosis, has allowed study of papillary pathophysiology and has shown a functional inter-relationship between the two sphincteric zones.     

Endoscopic manometry of the pancreatic duct and sphincter zone in patients with chronic pancreatitis

A possible mechanism for pain in alcohol-induced chronic pancreatitis is increased pancreatic duct pressure. A study has been done to compare sphincter of Oddi and pancreatic duct pressures in normal controls and patients with alcohol-induced chronic pancreatitis who had recently had pain or who were pain-free. Pressures were measured in the sphincter of Oddi in 10 controls and 33 patients, in the pancreatic duct in six controls and 15 patients, and in the common bile duct in four controls and five patients during station pull-through at the time of an endoscopic retrograde cholangiopancreatogram. There was no significant difference in the mean pressures in the pancreatic duct, sphincter of Oddi (basal and phasic), and frequency of papillary contraction when comparing patients with alcoholic pancreatitis and controls. There was also no difference between patients with or without pain and patients with or without strictures. This study has not confirmed the hypothesis that increased pancreatic duct pressures may be incriminated as a possible mechanism of pain in alcoholic-induced chronic pancreatitis.     

Endoscopic manometry of the sphincter of Oddi and pancreatic duct in patients with chronic pancreatitis

Summary Conclusion Endoscopic manometry in patients with chronic pancreatitis has demonstrated some manometric abnormalities in the sphincter of Oddi, but these abnormalities have no significant role in the pathogenesis of chronic pancreatitis. Background The study was undertaken to determine whether the sphincter of Oddi dysfunction plays a significant role in the pathogenesis of chronic pancreatitis. Methods Manometric investigation was performed in 32 patients with chronic pancreatitis. Twenty-three of them had alcohol-induced chronic pancreatitis, seven had biliary pancreatitis, and two patients had annular pancreas with chronic pancreatitis. Fifteen of them had dilated main pancreatic duct. Twenty-one cholecystectomized patients with no abnormality of the pancreas and biliary system served as controls. Results This study showed no significant difference in the mean pressures in the pancreatic duct, sphincter of Oddi (basal and phasic), and frequency of the sphincter of Oddi phasic contractions when comparing patients and controls. Sphincter of Oddi basal pressure (26–44 mmHg) was markedly increased in seven patients, whereas three patients (two of them had increased sphincter of Oddi basal pressure) had increased pancreatic duct pressure (20–24 mmHg). Increased numbers of retrograde contractions were found in seven patients.     

Effects of Gabexate Mesilate, a Protease Inhibitor, on Human Sphincter of Oddi Motility

Gabexate mesilate is an antiprotease drug, which reduced the severity of pancreatitis and frequency of post-ERCP pancreatitis. In dogs gabexate inhibits sphincter of Oddi motility but no data are available in humans. The aim of this study was to verify by manometry the action of gabexate on human sphincter of Oddi motility. We enrolled 12 patients with idiopathic recurrent pancreatitis (eight males, five females, mean age 46 ± 8 years). Standard preendoscopic sphincter of Oddi manometry was done in basal conditions and during infusion of gabexate 20 mg/min: basal pressure, amplitude and frequency of phasic contractions, and motility index (amplitude per frequency) were calculated before and after gabexate injection. Statistical analysis was performed by using Wilcoxon rank test for paired data. Six patients had a manometric diagnosis of stenosis (basal pressure greater than 40 mm Hg); six had normal findings. Phasic activity was not evaluable in five patients with stenosis. Basal pressure was unaffected by drug infusion, while gabexate caused a significant reduction of phasic activity, both in terms of frequency (4.5 ± 1 vs 3.6 ± 1; P < 0.05) and amplitude (157.4 ± 44 vs 80.0 ± 32; P < 0.05) of contractions. Motility index was reduced on average by 49%. In conclusion, this pilot study confirms, in patients with acute recurrent pancreatitis, the inhibitory action of gabexate on sphincter of Oddi motility already described in dogs. This action needs to be revaluated at therapeutic dosages. On the other hand, prophylactic use of the drug should be avoided during sphincter of Oddi manometry, in order to avoid false negative results.     

Manometric activity of the pancreatic duct sphincter in patients with total bile duct sphincterotomy for sphincter of Oddi dyskinesia

Previous anatomical studies have described a distinct sphincteric structure at the entrance of the common bile and pancreatic ducts in the duodenum. However, from an anatomical point of view, the pancreatic duct sphincter is only present in one third of human specimens. The purpose of the present study was therefore to investigate whether sphincteric activity could be demonstrated in patients in whom the common bile duct sphincter was completely transsected during endoscopic sphincterotomy. Twelve patients had a complete bile duct sphincterotomy because of sphincter of Oddi dyskinesia. The sphincterotomy was checked manometrically in all, and neutralization of the choledochoduodenal gradient recognized. In all patients a distinct pancreatic sphincteric zone with base-line elevation and superimposed phasic activity was demonstrated. In six patients the pancreatic duct sphincter was studied before and after bile duct sphincterotomy, and, although a definite sphincter zone still was present in the pancreatic duct, a reduction in phasic wave amplitude was observed. A similar decreased base-line and pancreatic duct pressure was observed, although not statistically significant.     

Bile duct dyskinesia. Clinical and manometric study

Unexplained right upper quadrant symptoms have often been attributed to bile duct dyskinesia. In this study we evaluated the pressure profile of the sphincter of Oddi in 10 patients with recurrent episodes of right upper quadrant pain, intermittent mild transaminasemia, and a normal pancreatobiliary tract. Nine healthy volunteers served as control. A triple-lumen catheter with an external diameter of 1.7 mm and recording sites at 2-mm intervals was introduced into the papilla through the endoscope. Ductal pressure, basal sphincter of Oddi pressure, and the amplitude and propagation direction of the phasic contractions of the sphincter were determined in patients and subjects. All measurements were performed relative to duodenal pressure, which was taken as zero. There was no significant difference between patients and subjects in the amplitude and frequency of phasic contractions of sphincter of Oddi. In contrast, the patients demonstrated a higher sphincter of Oddi pressure (p less than 0.005) and increased proportion of retrograde propagation direction of phasic contractions (p less than 0.01). It is concluded that a subpopulation of patients with unexplained abdominal pain demonstrated abnormal pressure profile of the sphincter of Oddi.     

Pressure measurements from biliary and pancreatic segments of sphincter of oddi

Using a minimally compliant infusion system and a triple-lumen pressure recording catheter, we obtained endoscopic manometric measurements from both the common bile duct and pancreatic duct segments of the sphincter of Oddi (SO) in 58 patients. Fifteen patients (ages 27–69) had the diagnosis of functional abdominal pain, 19 patients (ages 30–76) had partial biliary obstruction, and 24 patients (ages 15–80) had idiopathic acute recurrent pancreatitis. Resting ductal pressure was similar in the common bile duct and pancreatic duct in all patient groups. In the group with functional pain, basal SO pressure was similar, whether obtained from the common bile duct or pancreatic duct sphincteric segment. Eight of 19 patients with partial biliary obstruction had elevated basal SO pressure. Five of these eight patients had elevated basal SO pressure confined exclusively to the common bile duct segment of the sphincter, while three patients had elevated basal SO in both segments. Conversely seven of 24 patients with acute recurrent pancreatitis had an elevated basal SO pressure, with five patients having pressure elevation only in the pancreatic duct segment while two patients had abnormal basal SO pressure in both segments. We conclude that selective cannulation of the common bile duct and/or the pancreatic duct during manometric study of the SO is necessary in order to diagnose segmental SO dysfunction responsible for partial biliary obstruction or episodes of acute recurrent pancreatitis.     

Common bile duct pressure and Oddi sphincter pressure in patients with common bile duct stones with and without juxta-ampullar diverticula of the duodenum.

Resting common bile duct pressure and Oddi sphincter pressure were measured in 16 patients with common bile duct stones, 8 having in addition a juxta-ampullar diverticulum. Pressure measurements were performed with an infused catheter introduced through an endoscope under direct vision. No significant differences in fasting common bile duct pressures were observed between the two groups. The Oddi sphincter had a phasic activity, and the peak pressure was similar in both groups.