Effect of propofol on human sphincter of Oddi

The effect of propofol was studied in 11 patients who had common bile duct sphincter of Oddi manometry for suspected dysfunction. Patients were initially sedated with midazolam and then further or resedated with propofol for the second set of pressure measurements. Recordings were made about 10 min after giving each drug. No patient had elevated basal pressure initially. Average basal pressure was unchanged (16.7±16.4 mm Hg), phasic contraction frequency was unchanged (3.4±3.8/min), and phasic contraction amplitude fell but did not achieve statistical significance (91.8±77.3 mm Hg,P=0.1). There was no difference in lowest blood pressure, pulse, or oxygen saturation recorded during midazolam or propofol sedation. Subjectively, the patients were more sedated during propofol administration. It is concluded that propofol is a safe and effective agent for conscious sedation. It does not alter the sphincter of Oddi pressure profile in patients with normal basal sphincter pressures and thus could be used as an alternative and perhaps better form of sedation for ERCP with sphincter of Oddi manometry.Supported by a grant from Poudre Valley Hospital Foundation.     

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.     

Sphincter of oddi manometry in healthy volunteers

In this study we describe in detail the characteristics of sphincter of Oddi motor function in a large group of healthy subjects. Studies were obtained in 50 healthy volunteers. The findings showed a sphincter of Oddi segment that had a basal pressure of 14.8±6.3 mm Hg (X±sd). Phasic contractions were superimposed on the basal pressure. They had an amplitude of 119.7±32 mm Hg, a duration of 4.7±1 sec, and a frequency of 5.7±1.2 contractions/min. In 40 subjects the propagation sequence of phasic contractions could be evaluated and were simultaneous in 53%, antegrade in 35%, and retrograde in 11% of the waves. In 20 subjects, pressure measurements done at the common bile duct sphincter were similar to those obtained at the pancreatic duct sphincter. In 10 subjects, pressure values obtained at the common bile duct sphincter within a week were similar. Our study should help to establish standards for normal manometric values of the sphincter of Oddi and emphasizes the importance of having a healthy volunteer group from which to obtain the normal values of sphincter of Oddi motor function.     

Controlled study of the effect of nicardipine and ceruletide on the sphincter of Oddi.

Although sphincter of Oddi dysfunction is a recognised cause of post cholecystectomy pain, the control mechanisms involved in sphincter of Oddi function are poorly understood. Pharmacological relaxation of the sphincter of Oddi may have a beneficial effect particularly in sphincter of Oddi dysfunction where basal sphincter pressure is high. The aim of this study was to investigate the effects of calcium channel blockade (nicardipine) and synthetic cholecystokinin (ceruletide) on sphincter of Oddi pressures. Nineteen patients (median age 49 years; range 21-75) attending for routine endoscopic retrograde cholangiopancreatographic (ERCP) examination were studied. No patients with evidence of sphincter of Oddi dysfunction were included in the study. Each patient was randomly allocated to receive a three minute intravenous infusion of nicardipine 3 mg (six) ceruletide 5 ng/kg (seven) or placebo (six). Endoscopic biliary manometry was done with recording of basal sphincter of Oddi pressures, sphincter of Oddi phasic wave amplitude and frequency before and after intravenous infusions. In the nicardipine group patients showed a decrease in both basal and phasic amplitude sphincter of Oddi pressure (mm Hg) from the preinfusion values (mean (SEM)) of 24.7 (3.6) and 112.3 (13.4) to 12.9 (2.9) (p less than 0.01) and 89.9 (12.4) (p less than 0.03) after infusion respectively. Ceruletide produced a decrease in sphincter of Oddi phasic wave frequency (c/min) from 3.4 (0.3) before infusion to 2.6 (0.5) after infusion (p less than 0.05). We conclude that nicardipine effectively decreases sphincter of Oddi pressure. This drug may therefore be of value in the treatment of sphincter of Oddi dysfunction where raised sphincter pressures are thought to be the primary pathogenic feature.     

Effect of gastric distension and duodenal fat infusion on biliary sphincter of oddi motility in healthy volunteers

Although sphincter of Oddi (SO) dysfunction has been implicated in the pathogenesis of postcholecystectomy syndrome and pancreatitis, little is known about normal physiologic stimuli, such as intraduodenal fat on human SO motility. Furthermore, gastric distension that frequently accompanies endoscopic manometry has been shown in animal studies to affect SO motility. We evaluated the effects of intraduodenal fat and gastric distension on SO basal pressure. Asymptomatic volunteers had SO manometry performed while sequentially performing gastric distension and intraduodenal fat perfusion. Five subjects (ages 29.8±4.8 years, range 22–35 years) had a mean basal sphincter of Oddi pressure of 23.4±5 mm Hg (range 17–31 mm Hg). Injection of air into the stomach caused no appreciable change in either intragastric pressure or SO pressure. Intraduodenal fat infusion resulted in a decrease in mean SO basal pressure from 23.4±5.0 to 4.4±4.4 mm Hg (P=0.004). These results demonstrate that gastric distension does not affect SO basal pressure and that intraduodenal fat infusion reduces SO basal pressure.This work was presented in part at the Digestive Disease Week in Boston, Massachusetts, in May 1993.This work was supported in part by a research award from the American Society of Gastrointestinal Endoscopy.     

Effect of octreotide on sphincter of oddi motility in patients with acute recurrent pancreatitis

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.     

A controlled study of the effect of midazolam on abnormal sphincter of Oddi motility

BACKGROUND: The effect of a medication on sphincter of Oddi motility should be characterized if it is to be used during sphincter of Oddi manometry. Controversy exists as to whether midazolam influences sphincter of Oddi motility. This study assessed the effect of midazolam on the hypertensive sphincter of Oddi. METHODS: The study population consisted of 36 patients who presented with recurrent abdominal pain resulting from sphincter of Oddi dysfunction. The study was nonrandomized, prospective, and placebo controlled. Patient allocation was consecutive. Sphincter of Oddi manometry was performed in standard fashion. Manometric tracings were interpreted while the investigator was blinded to treatment allocation. Eighteen patients in the test group received 2 mg of midazolam intravenously whereas the 18 patients in the control group received saline solution intravenously. Manometric parameters were measured before and 3 minutes after the intravenous infusion. Changes in manometric findings before and after the administration of saline solution and midazolam were compared. RESULTS: Midazolam caused a significant reduction in basal sphincter of Oddi pressure (24 mm Hg) as compared with saline solution (p < 0.001). Diagnostic concordance (normal vs. abnormal) between the basal sphincter pressure before and after midazolam was seen in only 77% of patients. CONCLUSIONS: Midazolam significantly altered sphincter of Oddi motility. The decrease in sphincteric pressures would have altered diagnosis and management in 4 of 18 patients. Midazolam should not be used during sphincter of Oddi manometry.     

Effects of atropine and pirenzepine on sphincter of Oddi motility. A manometric study

We studied the Oddi sphincter motility by endoscopic manometry in 10 consecutive patients randomized in a double-blind fashion, after i.v. administration of two anticholinergic compounds (0.5 mg atropine sulfate and 10 mg pirenzepine). Pirenzepine significantly decreased the basal sphincteric pressure, as well as the amplitude and frequency of the phasic contractions. The only significant effect of atropine was the modification of the frequency of the phasic contractions, but only for a short period of time. Our results suggest that muscarinic innervation must be present for a normal sphincter of Oddi motility.     

Paradoxical response of sphincter of Oddi to intravenous injection of cholecystokinin or ceruletide. Manometric findings and results of treatment in biliary dyskinesia.

Sixty two patients with a clinical suspicion of biliary dyskinesia were investigated with endoscopic manometry of the sphincter of Oddi before and after intravenous injection of cholecystokinin or ceruletide. In 52 patients injection was followed by decreased pressure in the sphincter of Oddi; 43 of these had normal prestimulatory values (group I), while the values were raised in the other nine patients (group II). A paradoxical response to intravenous injection was observed in 10 women (group III): increased baseline sphincteric pressure occurred in eight and increase in the amplitude of phasic contractions in four patients. The prestimulatory sphincteric pressure was raised in five and normal in the remaining patients. Eight patients were treated with papillotomy (seven) or balloon dilatation of the sphincter (one). They experienced relief of pain during a follow up period of 11-16 months. Intravenous injection of cholecystokinin or ceruletide may disclose a special type of biliary dyskinesia even in patients with normal prestimulatory manometric findings. Hormone injection increases the diagnostic yield of endoscopic manometry in patients suspected of biliary dyskinesia.     

Effect of local instillation of alcohol on sphincter of Oddi motor activity: combined ERCP and manometry study

The effect of local instillation of alcohol on sphincter of Oddi motor activity was determined by endoscopic manometry. Sphincter of Oddi pressures and motor function were compared in eight cholecystectomized subjects with normal sphincter of Oddi motor function and in four patients with chronic alcoholic pancreatitis. The effect of local instillation of 3 ml of 40% alcohol was compared with water instillation. In cholecystectomized subjects, alcohol produced a significant increase of basal sphincter of Oddi pressure from 21.0 +/- 2.8 mm Hg to 95.8 +/- 83 mm Hg (p less than 0.01) without significant changes in the amplitude, duration, and frequency of phasic contractions. In patients with alcoholic chronic pancreatitis, alcohol instillation resulted in a significant increase of basal sphincter of Oddi pressure from 32.5 +/- 4.8 mm Hg to 225.1 +/- 105 mm Hg without changes in amplitude, duration, and frequency of phasic contractions. Two patients with chronic alcoholic pancreatitis had a tonic contraction of the sphincter of Oddi with transitory and mild epigastric pain. Local instillation of alcohol increases sphincter of Oddi motor activity which may play a role in the pathogenesis of alcoholic pancreatitis.     

Effect of nalbuphine on the motility of the sphincter of Oddi in patients with suspected sphincter of Oddi dysfunction

BACKGROUND: Nalbuphine is an ideal supplementary analgesic drug for midazolam-induced conscious sedation during operative endoscopy because it has no cardiovascular effect and only a moderate depressive effect on respiration. However, no data are available as to whether nalbuphine is suitable as an analgesic drug during endoscopic sphincter of Oddi manometry. The aim of the present study was to investigate the effect of nalbuphine on the sphincter of Oddi motility in patients with a suspected sphincter of Oddi dysfunction. METHODS: Seventeen patients who were suspected clinically to have SOD after cholecystectomy were prospectively investigated. Five mg of midazolam was administered intravenously before the procedure to induce conscious sedation. After approximately 5 minutes of stationary sphincter of Oddi manometry recording (baseline), either 10 mg of nalbuphine or saline solution (placebo) was administered intravenously in random fashion and pressure was recorded for a further 5 minutes. Maximum sphincter of Oddi basal pressure and average phasic contraction amplitude and frequency were measured before and after the infusion of the drug or saline solution. RESULTS: Nalbuphine administration effectively enhanced the sedation obtained with midazolam without any adverse effect. When the sphincter of Oddi manometric periods before and after the administration of nalbuphine versus placebo were compared, there was a significantly increased basal sphincter of Oddi pressure only in the nalbuphine group: respectively, 49 (18) and 77 (29) mm Hg (p = 0.003) versus 51 (24) and 49 (23) mm Hg (p = 0.9). The phasic contraction amplitude did not change in response to nalbuphine, but the phasic contraction frequency increased significantly, from 5 (3) to 8 (4) per minute (p = 0.04). CONCLUSIONS: Nalbuphine has a stimulatory effect on sphincter of Oddi motility in patients with a suspected sphincter of Oddi dysfunction. Nalbuphine should not be used as premedication before endoscopic ERCP if sphincter of Oddi manometry is to be performed.     

Reproducibility of endoscopic sphincter of Oddi manometry

Results from endoscopic sphincter of Oddi manometry are being used to support the diagnosis of sphincter dysfunction in patients with unexplained pain after cholecystectomy. However, there are few data on the reproducibility of manometric records or motility diagnosis during a second test. In this study, the reproducibility of manometric records was assessed in 12 patients with pain after cholecystectomy by performing a second study after three months. Manometric tracings were evaluated without access to patients details and scored for sphincter basal pressure, frequency and amplitude of phasic contractions, propagation of phasic contractions, and responses to intravenous injection of cholecystokinin octapeptide (20 ng/kg). At the initial manometric study, four patients were diagnosed as normal, four as stenotic, and four as dyskinetic. Those diagnosed as normal and stenotic at the first study had an identical diagnosis at the second study. However, the diagnosis of dyskinesia was reproduced only in two of the four patients. In the other two patients a diagnosis of "stenosis" and "normal" was made at the second study. Cholecystokinin octapeptide (20 ng/kg intravenous bolus) produced inhibition of phasic contractions in all studies, both initially and at three months. We conclude that endoscopic sphincter of Oddi manometry is reproducible when the initial diagnosis is either normal or stenosis. However, the diagnosis of dyskinesia is poorly reproducible, perhaps due to the episodic nature of this manometric disorder or to progression of sphincter of Oddi dysfunction.     

Effects of intraduodenal air insufflation on sphincter of oddi motility in conscious dogs

To investigate effects of intraduodenal air insufflation on sphincter of Oddi motility, manometric recordings were obtained during fasting from the sphincter and duodenum in four conscious dogs with duodenal cannula. At 40% of the mean cycle length of the migrating motor complex predetermined from baseline recording, 160 ml of air was injected into the duodenum. In both the sphincter and duodenum, air insufflation produced premature phase III-like activity in seven of 20 experiments (35%) or nonspecific excitatory reaction in eight (40%). In the remaining five experiments (25%), the sphincter exhibited a transient inhibitory response, while the duodenum showed the nonspecific excitatory reaction. Basal pressure of the sphincter increased immediately after air insufflation in 90% of the 20 experiments. The mean basal pressure increased from 12.3±1.6 mm Hg to 22.4±2.1 mm Hg (P<0.0001) and minimum basal pressure from 2.9±0.9 mm Hg to 4.7±0.8 mm Hg (P<0.001). These results indicate that intraduodenal air insufflation does affect motility of the sphincter of Oddi and duodenum in conscious dogs.This work was presented at the 96th Congress of the Japanese Surgical Society on April 10–12, 1996, in Chiba, Japan.     

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.     

Does intrabiliary pressure predict basal sphincter of Oddi pressure? A study in patients with and without gallbladders

Background: The endoscopic measurement of sphincter of Oddi pressure is a technically difficult procedure requiring significant expertise. Intrabiliary pressure is technically easy to measure. Furthermore, since it is believed that the pathogenesis of pain in patients with sphincter of Oddi dysfunction is attributable to increased intrabiliary pressure, its measurement may be more clinically relevant than measurement of sphincter of Oddi pressure. Methods: Intrabiliary pressures were blindly measured in 54 patients who had sphincter of Oddi manometry for abdominal pain. Results: In all patients intrabiliary pressure was significantly higher in patients with sphincter of Oddi dysfunction than those with normal sphincter of Oddi pressure (19.6 ± 2.2 vs 9.6 ± 1.2 mm Hg; p < 0.01). These findings were similar when patients were stratified according to presence of intact gallbladder (19.3 ± 1.6 vs 8.8 ± 1.4; p < .001) and to patients without a gallbladder (20.1 ± 3.8 vs 12/1 ± 1.3; p = .034). There was positive correlation between intrabiliary pressure and sphincter of Oddi basal pressure. This correlation was significant both in patients with and without gallbladders. Conclusions: These data suggest that increased intrabiliary pressure may be a useful surrogate marker of sphincter of Oddi dysfunction. (Gastrointest Endosc 1996;44:696-9.)     

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.     

Prospective evaluation of droperidol on sphincter of Oddi motility

BACKGROUND: Droperidol increasingly is used as an effective adjunct for conscious sedation during endoscopic procedures. Given the concern for the effects of narcotics and benzodiazepines on sphincter of Oddi motility, and the potential difficulty in sedating patients undergoing sphincter of Oddi manometry, droperidol could be an ideal agent in this setting. METHODS: Over a 43-month period, consecutive patients undergoing sphincter of Oddi manometry were studied prospectively. Sphincter of Oddi manometry was performed under general anesthesia in all but 10 patients. Standard retrograde pull-through techniques were used to examine the biliary and/or pancreatic sphincter, depending on the indication for sphincter of Oddi manometry. After the initial two pull-throughs, 5 mg of droperidol were given intravenously and measurements were repeated 5 minutes later. RESULTS: A total of 55 patients were studied (42 women [76%], 13 men; mean age 43 years). The basal biliary sphincter pressures measured in 35 patients before and after droperidol were, respectively, 56 mm Hg and 48 mm Hg (p = 0.02); the basal pancreatic sphincter pressures measured in 22 patients before and after droperidol were, respectively, 92 mm Hg and 67 mm Hg (p = 0.29). By using a definition for sphincter of Oddi dysfunction of a basal pressure greater than 40 mm Hg, droperidol would have resulted in a change in diagnosis in 5 patients undergoing biliary manometry (one misclassified as sphincter of Oddi dysfunction, 4 misclassified as normal), and 6 patients undergoing pancreatic sphincter manometry (5 misclassified as sphincter of Oddi dysfunction, one misclassified as normal) (total 19% of procedures). No complication was associated with droperidol use. CONCLUSIONS: Droperidol alters basal sphincter pressures, which in some patients was clinically significant and would have resulted in misclassification. Although safe and well tolerated, droperidol appears to have subtle but clinically significant effects on the sphincter of Oddi.     

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.     

Biliary, Pancreatic, and Sphincter of Oddi Electrical and Mechanical Signals Recorded During ERCP

Measurements of biliary tract motility havefocused on radiologic and pressure measurements toquantify biliary motility rather than measurements ofelectrical activity of the biliary tract. We previously reported the recording of biliary electricalsignals during ERCP and now report on the continueddevelopment and validation of a system to measurebiliary tract electrical activity as well as biliarymechanical activity. In 26 patients presenting with avariety of clinical indications, we recordedmeasurements of electrical activity from the common bileduct sphincter (16 patients), pancreatic duct sphincter(eight patients), and/or sphincter of Oddi (eightpatients). Electrical recordings were performed with aspecially modified ERCP catheter, using two circularelectrodes as well as a custom catheter that measured both electrical and mechanical activity.Electrical activity of the biliary tract wassuccessfully recorded in 25 of 26 patients (96%),including the common bile duct sphincter (16 patients,62%), pancreatic duct sphincter (eight patients, 31%) andsphincter of Oddi (eight patients, 31%). Along with theelectrical recordings, common bile duct sphinctermechanical activity was recorded in 12 patients (67%), pancreatic duct sphincter mechanical activityin six patients (33%), and sphincter of Oddi mechanicalactivity in six patients (33%). Frequency analysis ofelectrical signals revealed a mean frequency(cycles/min) of 4.7 ± 0.5 in the common bile ductsphincter, 4.1 ± 0.6 in the pancreatic ductsphincter, and 4.9 ± 0.7 in the sphincter ofOddi. Phasic mechanical frequency in cycles per minutewas recorded at a frequency of 4.8 ± 0.5 in common bileduct sphincter, 4.0 ± 0.6 in pancreatic ductsphincter, and 5.3 ± 0.9 in sphincter of Oddi.Tonic pressure (averaged 12.1 ± 1.5 mm Hg) incommon bile duct sphincter, 12.4 ± 1.4 mm Hg inpancreatic duct sphincter, and 15.0 ± 5.1 mm Hgin sphincter of Oddi. Analysis of wave form propagations(noted as percentage antegrade, retrograde, orindeterminant) revealed 50% antegrade, 23% retrograde, and 27%indeterminant). One patient was recorded on twooccasions via ERCP; the same patient had anintraoperative recording. All three recordings showedsimilarities. We conclude that measurements of biliary,pancreatic, and sphincter of Oddi electrical andmechanical activity are feasible and can be done as partof ERCP. There was good correlation between biliarytract electrical and mechanical events and differentwave form characteristics were noted for different partsof the biliary tree. Further studies are warranted toevaluate the potential usefulness of measurement of biliary tract electrical activity, and toconfirm its correlation with mechanical events in thepancreato-biliary tree.     

Aerobilia and hypomotility of the sphincter of Oddi in a patient with chronic intestinal pseudo-obstruction.

A 50-year-old woman with a typical history of chronic idiopathic intestinal pseudo-obstruction was admitted to hospital because of an acute episode of abdominal cramps, nausea, and vomiting. The diagnosis of chronic idiopathic intestinal pseudo-obstruction had been established in this patient who had malnutrition and extreme weight loss as a result of severe malabsorption syndrome. The abdominal roentgenogram showed a typical hypotonic intestine with an enlarged stomach and distended intestinal loops with the radiological signs of an ileus. In addition to former episodes, there was also a transient aerobilia. The patient had not undergone biliary surgery or endoscopic sphincterotomy. To investigate the cause of the findings, endoscopic retrograde cholangiopancreatography and endoscopic manometry of the sphincter of Oddi were performed. The endoscopy showed the stomach and duodenum with a wide and dilated lumen and no spontaneous motility. Endoscopic manometry of the biliary tract and the sphincter of Oddi showed several abnormalities compared with a group of normal volunteers or patients who were examined via biliary manometry for other reasons. There was a low basal pressure (3.5 mm Hg) in the sphincter of Oddi together with low-amplitude phasic contractions (25-30 mm Hg), but the contraction frequency was in the normal range. Further investigations of the motility of the gastrointestinal tract in this patient showed diffuse esophageal spasms and a markedly delayed gastric emptying. The findings of biliary manometry in this patient suggest involvement of the sphincter of Oddi and the biliary system in chronic idiopathic pseudo-obstruction.