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PubMed1998

Endoscopic injection of botulinum toxin for biliary sphincter of Oddi dysfunction.

BACKGROUND AND STUDY AIMS: Endoscopic sphincterotomy is not without risks, and is also ineffective in about half of patients with type III sphincter of Oddi dysfunction (SOD), i.e. those without clinical evidence of biliary obstruction (normal liver tests, normal bile duct diameter, and regular drainage time at endoscopic retrograde cholangiography). The present study therefore investigated the efficacy and safety of endoscopic botulinum toxin (BTX) injection into the papilla of Vater, and analyzed whether the symptomatic response to BTX injection might be a predictor of outcome for endoscopic sphincterotomy. PATIENTS AND METHODS: Twenty-two patients who had undergone cholecystectomy and had manometrically confirmed type III SOD were enrolled during a three-year study period. All patients received treatment with an endoscopic single-shot injection of 100 mouse units of BTX into the papilla of Vater. Initial symptomatic responses were analyzed six weeks later. If the BTX injection had been ineffective, or if biliary symptoms recurred after initial benefit during the follow-up period, endoscopic manometry and endoscopic sphincterotomy were performed. All patients then received further prospective clinical follow-up examinations. RESULTS: With the exception of one patient with mild pancreatitis (4.5%), no side effects were observed after endoscopic BTX injection. Six weeks after BTX injection, 12 SOD patients (55%) were symptom-free, but ten patients (45%) were not. However five of these ten SOD patients who did not experience symptomatic benefit from BTX injection had normal basal sphincter of Oddi pressures (< 40 mmHg) at this time, and none of these five patients was free of complaints after subsequent endoscopic sphincterotomy. Two of the remaining five patients with sustained sphincter hypertension after BTX injection benefitted from endoscopic sphincterotomy. Eleven of the 12 SOD patients who had initially responded to BTX injection developed recurrent symptoms after a median period of six months. Manometry revealed sphincter hypertension in all 11 cases, and all patients became free of complaints again after endoscopic sphincterotomy during a median follow-up of a further 15 months. Overall, 11 of the 12 patients who responded to BTX injection, versus two of the ten patients who did not gain pain relief after BTX injection, later benefitted from endoscopic sphincterotomy (p < 0.01). CONCLUSIONS: Endoscopic injection of botulinum toxin into the papilla of Vater is a safe procedure and provides short-term relief of symptoms in half of patients with type III SOD. Our results also indicate that the clinical response to BTX injection can predict whether SOD patients will gain long-term benefit from endoscopic sphincterotomy.

Adult↗
PubMed1989

[Oddi's sphincter dysfunction].

Dysfunction of the sphincter of Oddi (SOD) is an uncommon condition which must be considered in cases of persistent pain in the upper abdomen following uncomplicated cholecystectomy, when disease in other organs, such as gastric ulcer, esophagitis and pancreatitis has been eliminated. The pathogenesis is not fully elucidated, but it is assumed that the cholecystectomy in some cases induces an increased tendency to spasm in the sphincter of Oddi (SO), and, perhaps in connection with an increased sensitivity to pressure elevations in the biliary tree, results in attacks of pain. Whether fibrosis (stenosis) of the SO due to instrumentation or passage of stones is part of the etiology is obscure. Endoscopic retrograde cholangiopancreaticography with papillary manometry should be performed in all cases where SOD is suspected. An elevated basal pressure in SO seems to be the best indicator of SOD. In cases unresponsive to conservative treatment, endoscopic sphincterotomy may be considered. This treatment is not finally evaluated, but apparently the effect is good, especially in patients with elevated basal pressure in SO. It is emphasized that the knowledge of the behavior and regulation of SO is incomplete and that this should be remembered when criteria for SOD are applied.

Ampulla of Vater↗
PubMed1994

Efficacy of quantitative cholescintigraphy in the diagnosis of sphincter of Oddi dysfunction.

The diagnostic efficacy of time-activity curves (TAC) and common bile duct dynamics (CBDD) derived from quantitative cholescintigraphy (QC) was assessed in patients with suspected sphincter of Oddi dysfunction (SOD). Quantitative cholescintigraphy was performed on 34 cholecystectomized individuals with suspected SOD and 26 asymptomatic controls. Each patient with suspected SOD underwent endoscopic retrograde cholangiography and sphincter of Oddi manometry (SOM). After exclusion of eight patients because of failure of manometry, the final diagnoses of the remaining 26 patients were taken as the gold standard by which to determine the detectability of TAC and CBDD. The sensitivity of TAC reached 68.8%. Common bile duct dynamics showed equal sensitivity but was more specific than TAC. The sensitivity improved to 87.5% when TAC and CBDD were combined. We conclude that non-invasive QC provides good sensitivity and specificity in evaluating cholecystectomized patients with suspected SOD.

Aged↗
PubMed1994

Endoscopic sphincterotomy-induced pancreatitis: increased risk associated with nondilated bile ducts and sphincter of Oddi dysfunction.

OBJECTIVE: to evaluate the relationship between common bile duct diameter and the risk of sphincterotomy-induced pancreatitis. METHODS: Two hundred and ten consecutive patients were prospectively investigated. Patients were divided into three groups according to the indication for sphincterotomy: Group I had common bile duct stones (n = 108), group II had sphincter of Oddi dysfunction (n = 48), and group III had sphincterotomy for other indications (n = 54) (i.e., stent, dilation). RESULTS: There were 62 males and 148 females with a mean age of 60 yr (range 15-93 yr). Eleven of the 210 patients (5.2%) developed pancreatitis. Other sphincterotomy-induced complications were bleeding (n = 2), cholangitis (n = 2), retroperitoneal duodenal perforation (n = 1), and bile duct leakage (n = 1). The percentages of pancreatitis in groups I (3.7%), II (12.5%), and III (1.9%) were significantly different (p = 0.03). Patients with nondilated common bile ducts (< or = 10 mm) had more pancreatitis than patients with dilated common bile ducts (8.8% vs. 2.8%), but the difference was not significant (p = 0.07). However, when group III was excluded from the analysis, there was a significant difference in the percentage of pancreatitis between the patients with nondilated bile ducts and those patients with dilated bile ducts (13.1% vs. 2.2%, respectively; p < 0.01). Analysis for trend did not show a significant inverse relationship between bile duct diameter and the rate of sphincterotomy-induced pancreatitis. However, for all complications combined, the inverse relationship between bile duct diameter and rate of sphincterotomy-induced complications was significant: < or = 5 mm (23.1%), > 5-10 mm (13.8%), > 10-15 mm (3.2%), > 15 mm (2.4%) (p = 0.002). CONCLUSIONS: Endoscopic sphincterotomy is more hazardous in patients with nondilated bile ducts and sphincter of Oddi dysfunction. Further studies are needed to determine whether pancreatic stenting reduces the risk of sphincterotomy-induced pancreatitis in those clinical settings.

Common Bile Duct↗
PubMed1999

Clinical aspects of sphincter of Oddi function and dysfunction.

The sphincter of Oddi (SO) functions to regulate the flow of bile and pancreatic juices as well as to prevent the reflux of duodenal contents into the pancreatobiliary system. When dysfunction of the sphincter occurs, symptoms develop relating to either the biliary or pancreatic portions of the sphincter. The mechanism of this dysfunction remains speculative. SO manometry remains the "gold standard" to correctly diagnose the disorder and stratify therapy. Division of the sphincter is effective for SO stenosis, but there is no proven therapy for SO dyskinesia.

Bile↗
PubMed2001

Concomitant manifestation of achalasia and sphincter of Oddi dysfunction.

We report the case of a 44-year-old woman who suffered from biliary-type pain after cholecystectomy, dysphagia, and weight loss. Examinations revealed sphincter of Oddi dysfunction (SOD) and achalasia. Complete relief of symptoms was achieved by endoscopic sphincterotomy and pneumatic dilation of the distal esophagus. This case report demonstrates for the first time the concomitant manifestation of two motility disorders of the upper gastrointestinal tract, i.e. achalasia and SOD. At present, any causal relationship seems speculative; however, both diseases were successfully treated using endoscopic procedures.

Adult↗
PubMed1995

Common bile duct sphincter of Oddi stenting in patients with suspected sphincter dysfunction.

OBJECTIVES: Some patients seem to have symptoms or other findings that imply that they have sphincter of Oddi dysfunction, but when the sphincter pressure is measured, the basal resting pressure is not greater than 40 mm Hg. Because empiric sphincterotomy can alleviate some of these patients'symptoms, it is suspected that they have intermittent spasm or dysfunction. Prolonged stenting of the sphincter would prevent symptoms in patients with this intermittent disorder. Thus, one could determine which patients would benefit from a sphincterotomy without subjecting all the patients to the risk of sphincterotomy. METHODS: Twenty-one patients with suspected sphincter of Oddi dysfunction were studied. All had basal sphincter of Oddi pressures < 40 mm Hg. The gallbladder was in situ in three. The others had persistent abdominal pain after cholecystectomy. Benefit was defined as no symptoms for 2 months after stent placement, followed by continued lack of symptoms once a sphincterotomy was performed. RESULTS: Nine patients benefited and 12 did not. One relapsed, but benefited from a repeat sphincterotomy. Eight patients (38%) met criteria for pancreatitis after stent placement. Two had severe pancreatitis with pseudocyst development. There were no sphincterotomy-related complications. CONCLUSIONS: The results suggest that patients without basal resting sphincter of Oddi pressure criteria may have intermittent spasm or dysfunction which can be deduced by achieving benefit after stenting, but the risk of pancreatitis from this technique as described is too high to recommend stenting as a routine method for detecting patients with intermittent sphincter dysfunction/spasm. Alternate methods need to be developed to identify these patients.

Abdominal Pain↗
PubMed2000

Sphincter of Oddi function and dysfunction.

The sphincter of Oddi (SO) is situated at the junction of the bile and pancreatic ducts where they enter the duodenum, and it serves to regulate the flow of bile and pancreatic juices as well as to prevent the reflux of duodenal contents into the pancreatobiliary system. SO dysfunction relates to either the biliary or pancreatic portions of the sphincter. Distinct clinical syndromes relating to either sphincter segment are recognized. The mechanism of dysfunction remains uncertain, but disruption of neural pathways involved in sphincter function seems likely. SO dysfunction is best diagnosed by manometry, which is able to correctly stratify patient groups and determine therapy. Biliary scintigraphy, which is noninvasive, has shown promise as a screening tool for patients with suspected SO dysfunction. Division of the sphincter is an effective treatment for patients with manometrically proven SO stenosis for either the biliary or pancreatic form of the disorder. Other forms of SO dysfunction may benefit from pharmacotherapy.

Common Bile Duct Diseases↗
PubMed1997

Small bowel dysmotility in patients with postcholecystectomy sphincter of Oddi dysfunction.

Postcholecystectomy patients (N = 27) with severe recurrent biliary-like pain who had no evidence of organic disease were subdivided into those with and those without objective evidence of sphincter of Oddi dysfunction (SOD) based on two separate criteria: (1) clinical criteria-elevated liver function tests and/or amylase with pain, and/or a dilated bile duct, and/or delayed drainage at ERCP (N = 14, SOD classes I and II); and (2) abnormal biliary manometry (N = 19). Prolonged (24-48 hr) ambulant recording of duodenojejunal motor activity was performed in all patients and interdigestive small bowel motor activity compared between patient subgroups and a healthy control group. Phase II motor abnormality was more frequent in patients with, compared to those without, objective clinical criteria of SOD (7/14 vs 0/13, P = 0.003). Phase III abnormality also tended to be more frequent in these patients (7/14 vs 2/13, P = 0.06). In addition, both phase III (P = 0.03) and phase II (P = 0.03) motility index (MI) was higher in patients with sphincter dyskinesia compared to controls; phase II MI was also higher in patients with sphincter stenosis (P = 0.005). Disturbances of small bowel interdigestive motor activity are more prevalent in postcholecystectomy patients with, compared to those without, objective evidence of SOD, and especially in patients with SO dyskinesia. Postcholecystectomy SOD in some patients may thus represent a component of a more generalized intestinal motor disorder.

Adult↗
PubMed2003

The relationship of bile duct crystals to sphincter of Oddi dysfunction.

Bile duct crystals collected either from the duodenum after gallbladder contraction or directly from bile duct aspiration are surrogates for gallbladder stones and microlithiasis. Whether bile crystals also serve as surrogates for bile duct stones or microlithiasis that forms in the bile duct after cholecystectomy is not known based on current data. Sphincter of Oddi dysfunction (SOD), due either to muscular spasm or sphincter fibrosis, is a cause of bile duct obstruction. Almost all of the literature on SOD involves patients who have had a prior cholecystectomy. Intuitively, obstruction at the SO following cholecystectomy would seem to lead to biliary stasis and predispose patients to bile duct microlithiasis. However, a recent study did not find bile duct crystals in patients with manometrically diagnosed SOD. The reason for this is unknown, although we hypothesize that cholesterol and bilirubinate crystals are not surrogates for brown pigment stones commonly found in patients following cholecystectomy.

Cholecystectomy↗
PubMed1995

Sphincter of Oddi dysfunction caused by an ampullary neoplasm.

The case of a 50-year-old man with abdominal pain and abnormal liver test results is described. Endoscopic retrograde cholangiopancreatography with manometric studies showed biliary dilatation, poor ductal drainage, and sphincter of Oddi dysfunction. Clinical and radiographic clues suggested the possibility of an ampullary lesion; a small ampullary adenoma was detected after endoscopic sphincterotomy, and ampullary carcinoma was found in the operative specimen. Malignancy can cause sphincter dysfunction not only in the esophagus (as pseudoachalasia) but in the ampulla of Vater as well.

Ampulla of Vater↗
PubMed1997

Discordance of pressure recordings from biliary and pancreatic duct segments in patients with suspected sphincter of Oddi dysfunction.

It remains controversial whether manometric parameters recorded from the pancreatic and biliary segment of the sphincter of Oddi (SO) differ. We therefore studied 48 consecutive patients (40 women, 43 +/- 11 years) with suspected SO dysfunction, in 33 of whom successful dual-duct SO manometry was obtained. Measures of concordance between the two duct segments were moderate for basal sphincter pressure (K = 0.31) and for contractile frequency (0.35), and were low for peak pressure (0.15) and for proportion of retrograde propagation (-0.19). There was also low concordance (-0.13) for the overall manometric diagnosis, and in 48% (CI 31-66%) of patients a conflicting diagnosis (normal/abnormal) was obtained from the two ducts. There was no evidence of a differential motor effect of CCK on either duct, nor were there significant differences in the rate of manometric abnormality according to the order of initial duct cannulation. These results indicate that, if technically feasible, dual-duct manometry of the sphincter of Oddi is required for diagnostic precision.

Adult↗
PubMedDate not supplied

Scintigraphic sign of functional biliary obstruction is pathognomic for sphincter of Oddi dysfunction.

BACKGROUND/AIMS: Quantitative hepatobiliary scintigraphy (QHBS) is a valuable method for the detection of a low-grade biliary obstruction in patients with suspected sphincter of Oddi (SO) dysfunction (SOD), though the relatively low specificity of this noninvasive test has been criticized. The aim of the present study was a critical assessment of the diagnostic value of glyceryl trinitrate-augmented QHBS in patients with suspected SOD. METHODOLOGY: Glyceryl trinitrate-augmented QHBS and endoscopic retrograde cholangiopancreatography (ERCP) was performed on 27 cholecystectomized patients with suspected SOD. RESULTS: In 14 patients the ERCP depicted organic causes of biliary obstruction (choledocholithasis, juxtapapillary diverticulum, Vater papilla adenoma and common bile duct stenosis). In 12 of the 13 patients with inconclusive ERCP, endoscopic SO manometry demonstrated an elevated SO basal pressure. In patients with manometrically confirmed SOD, glyceryl trinitrate administration significantly increased the radioactive bile transit into the duodenum and normalized the QHBS parameters. In contrast, the 14 patients with an organic biliary obstruction glyceryl trinitrate administration had no effect on the transpapillary bile flow. CONCLUSIONS: In conclusion, glyceryl trinitrate-augmented QHBS is a specific method in the diagnosis of SOD, proving the functional reversibility of the biliary obstruction.

Adult↗
PubMed1999

Sphincter of Oddi dysfunction after successful gallstone lithotripsy (postlithotripsy syndrome): manometric data and results of endoscopic sphincterotomy.

After successful gallstone lithotripsy, biliary pain recurs in about one third of patients. However, gallstone recurrence can be shown in only 40-60% of these patients. Therefore, other causes, such as sphincter of Oddi dysfunction (SOD), may be suspected. Twenty-two consecutive patients with recurrent biliary pain after successful gallstone lithotripsy without evidence of gallstone recurrence at ultrasonography were enrolled. Liver tests were elevated in 13 patients and ERC showed a dilated bile duct in nine. All 22 patients underwent sphincter of Oddi (SO) manometry, bile sample analysis for microlithiasis, endoscopic sphincterotomy (ES), and bile duct exploration with a Dormia basket. Thereafter, the patients were clinically followed at bimonthly intervals. SO manometry revealed SOD in 15/22 patients. This was more often the case in patients with initially larger (>2 cm) or multiple stones than after lithotripsy for solitary small stones (P < 0.01). Microlithiasis was detected in one patient, another patient had small biliary calculi at bile duct exploration (both without SOD). After ES, 14/15 patients with biliary SOD but none of the five without SOD improved (median follow-up: two years; P < 0.01). The one patient with CBD stones became symptom-free after ES, while the patient with microlithiasis improved after additional cholecystectomy only. Overall, ES proved to be the adequate therapy in 15/22 patients (68%, median follow-up: 22 months). After gallstone lithotripsy, SOD is found in about two thirds of patients with recurrent symptoms but without gallstone recurrence. In this group CBD stones or microlithiasis are rare. Therefore, SOD has to be suspected in this situation and ES gives favorable results, even when performed on a clinical basis only (without SO manometry).

Adult↗
PubMedDate not supplied

Long-term outcome after endoscopic sphincterotomy in patients with biliary colic and suspected sphincter of Oddi dysfunction.

Seventy-three highly selected patients (35 type II, 38 type III) with intractable biliary-type pain were studied with biliary manometry after a baseline endoscopic retrograde cholangiopancreatography was normal or showed only duct dilatation. No differences between the two groups were noted in regard to baseline sphincter hypertension (60% versus 55%), improvement after endoscopic sphincterotomy at mean follow-up of 3 years, or post-procedure pancreatitis rates (15% versus 16%). Although not statistically significant, a tendency for patients with bile ducts > or = 12 mm to have sustained clinical improvement after sphincterotomy was noted in comparison with patients having ducts < 12 mm; an inverse correlation between improvement in symptoms and presence of an intact gallbladder at baseline was also seen. The authors suggest that the current classification, which divides patients with recurrent right upper quadrant pain into types I, II, and III, is inadequate to define either incidence of sphincter of Oddi dysfunction or subsequent response to endoscopic sphincterotomy.

Biliary Dyskinesia↗
PubMedDate not supplied

[Oddi's sphincter dysfunction].

Since the first description by Glisson in 1681 many papers about the sphincter of Oddi have been published contributing to the understanding of its physiology. Sphincter manometry has brought to light new facts that allow a better understanding of old concepts such as the biliary dyskinesia and the post-cholecystectomy syndrome as well as a more rational evaluation of the clinical results of the sphincterectomy. A review of the physiologic, pharmacologic, diagnostic and therapeutic aspects of the dysfunction of the sphincter of Oddi is presented.

Adult↗