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Gallbladder ejection fraction and its relationship to sphincter of Oddi dysfunction.

Theoretically, relative distal common bile duct obstruction due to sphincter of Oddi dysfunction may be a cause of poor gallbladder evacuation observed on quantitative cholescintigraphy. In this study, the relationship of sphincter of Oddi dysfunction to the gallbladder ejection fraction by quantitative cholescintigraphy was explored. Eighty-one patients with biliary-type pain and otherwise normal evaluations underwent quantitative cholescintigraphy, sphincter of Oddi manometry, and ERCP. Abnormalities of stimulated quantitative cholescintigraphy and/or sphincter of Oddi manometry were present in 70% of this study group. Manometric evidence of sphincter dysfunction was present in patients with similar frequency irrespective of the degree of gallbladder evacuation. In conclusion, abnormalities of quantitative cholescintigraphy and sphincter manometry appear to be independent factors, although frequent findings in this patient population.

Adolescent↗

Gastrointestinal imaging update: swallowing disorders and sphincter of Oddi dysfunction.

This update focuses on swallowing disorders and sphincter of Oddi dysfunction. Anatomy and physiology of swallowing are described, as are the signs, symptoms, and etiology of swallowing disorders. The imaging of these patients, particularly with videofluoroscopic swallowing study and fiberoptic endoscopic examination of swallowing, is then discussed. Sphincter of Oddi dysfunction as a cause of postcholecystectomy syndrome as well as its classification is described. This is followed by an explanation of the roles of fatty meal sonography and hepatobiliary scintigraphy in patients with sphincter of Oddi dysfunction, particularly type II and type III.

Barium Sulfate↗

Outcome of endoscopic sphincterotomy in post cholecystectomy patients with sphincter of Oddi dysfunction as predicted by manometry and quantitative choledochoscintigraphy.

BACKGROUND: Sphincter of Oddi dysfunction is diagnosed at manometry and, after cholecystectomy, non-invasively at quantitative choledochoscintigraphy. Patients may benefit from endoscopic sphincterotomy. AIMS: The aim of this study was to assess the usefulness of choledochoscintigraphy compared with manometry in predicting outcome of sphincterotomy in post cholecystectomy patients with sphincter of Oddi dysfunction. PATIENTS AND METHODS: Thirty patients with biliary-type pain complying with the Rome diagnostic criteria of sphincter of Oddi dysfunction and belonging to biliary group I and II were subjected to clinical evaluation, choledochoscintigraphic assessment of the hepatic hilum-duodenum transit time, endoscopic retrograde cholangiopancreatography, and perendoscopic manometry. Twenty two biliary group I and II patients with prolonged hepatic hilum-duodenum transit times were invited to undergo sphincterotomy. Fourteen patients underwent sphincterotomy; eight refused. Clinical and scintigraphic assessments were performed at follow up. RESULTS: Hepatic hilum-duodenum transit time was delayed in all patients with manometric evidence of sphincter of Oddi dysfunction, in all biliary group I patients and in 64% of biliary group II patients. At follow up, all patients who underwent sphincterotomy were symptom free and hepatic hilum-duodenum transit time had either normalised or significantly improved. A favourable post sphincterotomy outcome was predicted in 93% of cases at choledochoscintigraphy and in 57% at manometry. CONCLUSIONS: Quantitative choledochoscintigraphy is a useful and non-invasive test to diagnose sphincter of Oddi dysfunction as well as a reliable predictor of sphincterotomy outcome in post cholecystectomy biliary group I and II patients, irrespective of clinical classification and manometric findings.

Adult↗

Sphincter of Oddi dysfunction: managing the patient with chronic biliary pain.

Sphincter of Oddi dysfunction (SOD) is a syndrome of chronic biliary pain or recurrent pancreatitis due to functional obstruction of pancreaticobiliary flow at the level of the sphincter of Oddi. The Milwaukee classification stratifies patients according to their clinical picture based on elevated liver enzymes, dilated common bile duct and presence of abdominal pain. Type I patients have pain as well as abnormal liver enzymes and a dilated common bile duct. Type II SOD consists of pain and only one objective finding, and Type III consists of biliary pain only. This classification is useful to guide diagnosis and management of sphincter of Oddi dysfunction. The current gold standard for diagnosis is manometry to detect elevated sphincter pressure, which correlates with outcome to sphincterotomy. However, manometry is not widely available and is an invasive procedure with a risk of pancreatitis. Non-invasive testing methods, including fatty meal ultrasonography and scintigraphy, have shown limited correlation with manometric findings but may be useful in predicting outcome to sphincterotomy. Endoscopic injection of botulinum toxin appears to predict subsequent outcome to sphincterotomy, and could be useful in selection of patients for therapy, especially in the setting where manometry is unavailable.

Botulinum Toxins↗

Sphincter of Oddi dysfunction.

Evidence continues to accumulate indicating that sphincter of Oddi dysfunction may give rise to cholestasis, pancreatitis, or upper abdominal pain syndromes. Diagnosis of such dysfunction may be inferred from noninvasive tests or more precisely defined by manometric studies. Both the biliary and pancreatic sphincters are commonly involved. If medical therapy is ineffective, sphincter ablation via endoscopy or laparotomy should be considered for highly symptomatic patients. Complication rates of invasive techniques remain relatively high and risk:benefit ratio should be carefully considered. Future research as to etiology, more defined pathophysiology, more accurate noninvasive evaluation, and optimal therapies are awaited.

Common Bile Duct Diseases↗

Intrapancreatic ductal pressure in sphincter of Oddi dysfunction.

OBJECTIVES: It is widely believed that sphincter of Oddi dysfunction (SOD) induces pancreatitis through an increase in intrapancreatic ductal pressure. Animal models have demonstrated that increased intrapancreatic ductal pressure plays a role in the development of pancreatitis. The role of intrapancreatic ductal pressure in SOD-induced pancreatitis has not been investigated in humans. The present study sought to (1) investigate the effect of SOD on intrapancreatic ductal pressure and (2) identify the correlation between elevated intrapancreatic ductal pressure and the presence of pancreatitis. METHODS: A total of 263 patients presenting with abdominal pain, acute recurrent pancreatitis, or chronic pancreatitis were studied. Intrapancreatic ductal pressure was measured blindly. Subsequently complete SOM was performed in standard fashion. RESULTS: Intrapancreatic ductal pressure correlated significantly with sphincter of Oddi (SO) basal pressure (correlation coefficient: 0.39, P < 0.01). Individuals with SOD had a significantly higher pressure (19.6 +/- 15.9 mm Hg) as compared with those with normal SO motility (11.1 +/- 7.9 mm Hg) (P < 0.001). This significant difference was observed in all subgroups (recurrent abdominal pain, acute recurrent pancreatitis, and chronic pancreatitis) (P < 0.01). Patients with acute recurrent pancreatitis or chronic pancreatitis did not show a significant elevation in their intrapancreatic ductal pressures when compared with those with recurrent abdominal pain alone. CONCLUSIONS: SOD leads to an increase in intrapancreatic ductal pressure. Increased PD pressure is not the sole determinant for the development of pancreatitis.

Adult↗

Complications of endoscopic sphincterotomy. A prospective series with emphasis on the increased risk associated with sphincter of Oddi dysfunction and nondilated bile ducts.

Mostly retrospective series with limited use of sphincter of Oddi manometry have indicated that early complications are more common when endoscopic sphincterotomy is performed for sphincter of Oddi dysfunction than for common duct stones. The current study was undertaken to prospectively evaluate the frequency and type of complications of endoscopic sphincterotomy performed for sphincter of Oddi dysfunction compared with endoscopic sphincterotomy performed for other conditions. Four hundred twenty-three patients underwent sphincterotomy for sphincter of Oddi dysfunction (166), common duct stone(s) (163), tumor (60), and miscellaneous reasons (34). Patients were observed in the hospital for at least 24 hours after the procedure, and 30-day follow-up data were obtained. The overall complication rate was 6.9%, but complications were more frequent when sphincterotomy was performed for sphincter of Oddi dysfunction than for all other indications (10.8% vs. 4.3%; P = 0.009). Precut sphincterotomy was more frequently required in the sphincter of Oddi dysfunction group (21.1% vs. 11.7%, P = 0.009) but was no more likely to result in a complication (6.2%) than standard sphincterotomy. The risk of a complication was considerable for a small-diameter common bile duct (less than or equal to 5 mm), particularly when sphincterotomy was performed for sphincter of Oddi dysfunction (37.5%). The overall 30-day mortality rate was 1.7%, but the procedure-related mortality rate was believed to be 0.2%. It is concluded that endoscopic sphincterotomy for sphincter of Oddi dysfunction is more hazardous than for other conditions, particularly when a small common bile duct is present.

Cholangiopancreatography, Endoscopic Retrograde↗

The underestimated role of opiates in patients with suspected sphincter of Oddi dysfunction after cholecystectomy.

AIMS: Pain recurrence after cholecystectomy is often attributed to sphincter of Oddi dysfunction, whose diagnostic criteria and treatments remain uncertain. We performed a retrospective study to assess the possible precipitating role of opiate ingestion in this setting. METHODS: The retrospective study of the files of 147 consecutive patients investigated for post-cholecystectomy syndrome by endoscopic ultrasonography and/or endoscopic retrograde cholangiography yielded 37 cases of suspected biliary-type sphincter of Oddi dysfunction. RESULTS: Thirteen patients (30%) with suspected sphincter of Oddi dysfunction had taken opiate-containing drugs 15 minutes to two hours (median 1 hr) before the onset of pain ("Opiate group"). When compared with the 23 patients having not taken opiates ("Non Opiate Group"), they were significantly younger (47 vs. 60 yrs), had a narrower common bile duct (5.0 vs. 7.7 mm), but had similar biochemical abnormalities and belonged to the same Milwaukee's classes, mainly class II. None of the patients in the "Opiate group" were submitted to retrograde cholangiography or endoscopic sphincterotomy vs. 52% and 39%, respectively of the patients of the "Non-Opiate Group". After a mean follow-up of 3.5 years, there were three recurrences of biliary-type pain (1 choledochal stone, and 2 suspected sphincter of Oddi dysfunction) in the "Opiate Group", and 2 (1 choledochal stone, 1 after codeine intake) in the "Non-Opiate Group". CONCLUSIONS: Opiate intake is a frequent cause of suspicion of sphincter of Oddi dysfunction after cholecystectomy, especially in young patients with a narrow common bile duct. A careful history taking is essential to avoid unnecessary and potentially harmful procedures.

Age Distribution↗

[Do ultrasound parameters allow diagnosis of biliary sphincter of Oddi dysfunction?].

UNLABELLED: A noninvasive test to prove sphincter of Oddi dysfunction is desired, because endoscopic manometry is technically demanding and not without risks. METHODS: 40 consecutive patients (n = 20 patients with, and n = 20 patients without enzymatic cholestasis) with suspected SOD were investigated both by ultrasonography (US; 3.5 MHz) and by endoscopic manometry. SOD was suspected at US if the extrahepatic bile duct diameter was > or = 9 mm and a further increase (at least > 0.5 mm) was observed after intravenous ceruletide (0.3 micrograms/kg b.w.). SOD was verified manometrically by a sphincter of Oddi basal pressure > or = 40 mmHg. Endoscopic sphincterotomy was performed if SOD was diagnosed by manometry. Thereafter, all patients were enrolled in a prospective follow-up (median: one year). RESULTS: At US SOD was suspected in eleven of 20 patients with cholestasis. SOD was confirmed manometrically in all of them but also in two further patients (13 of 20 patients with proven SOD). After EST twelve of 13 patients remained free from biliary symptoms. In the 20 patients without cholestasis SOD was suspected at US in five patients only. However, endoscopic manometry revealed SOD in eleven of 20 patients and proved sonographically presumed SOD in only three of five patients. After EST only three of eleven patients remained asymptomatic during follow-up (p < 0.05 vs. patients with cholestasis). Clinically important side effects were not observed after ceruletide administration, whereas postmanometry pancreatitis was observed in three of 40 patients. CONCLUSION: In patients with recurrent symptoms after cholecystectomy and enzymatic cholestasis SOD was reliably diagnosed by ultrasonography (sensitivity: 85%, specificity: 100%), and this finding may guide endoscopic sphincterotomy.

Adult↗

Sphincter of Oddi dysfunction is associated with chronic pancreatitis.

OBJECTIVES: Chronic pancreatitis can be caused by ductal obstruction resulting from cicatricial papillary stenosis, but sphincter of Oddi motility studies have been inconclusive in patients with established chronic pancreatitis. We sought to determine whether there is an association between papillary sphincter dysfunction and changes of early chronic pancreatitis. METHODS: Consecutive patients who underwent sphincter of Oddi manometry to investigate unexplained upper abdominal pain (n = 104) were assessed for evidence of chronic pancreatitis by pancreatic ductography, endoscopic ultrasound, and pancreatic fluid bicarbonate concentration. RESULTS: Sphincter of Oddi dysfunction patients were four times more likely (odds ratio = 4.6) to have evidence of chronic pancreatitis than were those without sphincter dysfunction (p = 0.01). Of 68 patients with sphincter of Oddi dysfunction, 20 (29%) had structural evidence of chronic pancreatitis. Twenty of 23 (87%) patients with chronic pancreatitis had sphincter of Oddi dysfunction. CONCLUSIONS: Sphincter of Oddi dysfunction is associated with changes of chronic pancreatitis in patients with unexplained pancreaticobiliary pain. Longitudinal follow-up is required to confirm these preliminary findings.

Adult↗

Intestinal dysmotility in patients with sphincter of Oddi dysfunction. A reason for failed response to sphincterotomy.

Sphincter of Oddi dysfunction (SOD) is associated with abdominal pain and is treated by sphincterotomy. Of 215 patients who underwent biliary sphincterotomy for SOD in our institution, 26 reported no improvement and 25 of those were found to have pancreatic sphincter dysfunction and subsequently underwent pancreatic septotomy. Nine patients remained symptomatic after the second intervention. Six of those nine patients, and seven of the 16 patients who improved after the septotomy, agreed to undergo an ambulatory duodenojejunal (DJ) manometry. DJ manometry was abnormal in four of the six symptomatic patients but only in one of seven patients who became asymptomatic after endoscopic treatment. We conclude that the persistence of symptoms after endoscopic ablation of the biliary and pancreatic sphincters is associated with abnormal intestinal motility, which may explain in part the lack of response to the endoscopic treatment.

Abdominal Pain↗

Therapy of sphincter of Oddi dysfunction.

Since its original description, the sphincter of Oddi (SO) has been a source of controversy. Its very existence as a distinct anatomic or physiologic entity has been disputed. Hence, it is not surprising that the clinical syndrome of SO dysfunction and its therapy are controversial areas. The association of SO dysfunction with functional disorders and irritable bowel syndrome has raised skepticism about the efficacy of treatment directed solely at the SO. Nevertheless, SO dysfunction is widely diagnosed and treated by physicians. This article focuses on the various treatment options for SO dysfunction.

Botulinum Toxins↗

Systematic review: sphincter of Oddi dysfunction--non-invasive diagnostic methods and long-term outcome after endoscopic sphincterotomy.

BACKGROUND: Sphincter of Oddi dysfunction is a benign, functional gastrointestinal disorder for which invasive endoscopic therapy with potential complications is often recommended. AIMS: To review the available evidence regarding the diagnostic accuracy of non-invasive methods that have been used to establish the diagnosis and to estimate the long-term outcome after endoscopic sphincterotomy. METHODS: A systematic review of English language articles and abstracts containing relevant terms was performed. RESULTS: Non-invasive diagnostic methods are limited by their low sensitivity and specificity, especially in patients with Type III sphincter of Oddi dysfunction. Secretin-stimulated magnetic resonance cholangiopancreatography appears to be useful in excluding other potential causes of symptoms, and morphine-provocated hepatobiliary scintigraphy also warrants further study. Approximately 85%, 69% and 37%, of patients with biliary Types I, II and III sphincter of Oddi dysfunction, respectively, experience sustained benefit after endoscopic sphincterotomy. In pancreatic sphincter of Oddi dysfunction, approximately 75% of patients report symptomatic improvement after pancreatic sphincterotomy, but the studies have been non-controlled and heterogeneous. CONCLUSIONS: Patients with suspected sphincter of Oddi dysfunction, particularly those with biliary Type III, should be carefully evaluated before considering sphincter of Oddi manometry and endoscopic sphincterotomy. Further controlled trials are needed to justify the invasive management of patients with biliary Type III and pancreatic sphincter of Oddi dysfunction.

Common Bile Duct Diseases↗

Sphincter of Oddi dysfunction. Dynamic cholescintigraphy and endoscopic retrograde cholangiopancreatography with papillotomy in diagnosis, treatment, and follow-up study.

The study compares dynamic cholescintigraphy with traditional methods in diagnosing sphincter of Oddi dysfunction. Five patients with dysfunction of the sphincter, in accordance with traditional diagnostic criteria, are compared with 25 patients with postcholecystectomy syndrome. Dynamic cholescintigraphy showed complete separation of the two groups, T1/2 distinguishing better than Tmax. The patients with sphincter dysfunction were treated with endoscopic papillotomy (EPT) for symptomatic relief. Three had early complications. At follow-up study the courses were uneventful. Their symptoms had disappeared or markedly improved, and dynamic cholescintigraphy was normalized. In conclusion, dynamic cholescintigraphy seems to be a reliable noninvasive method for identification and control of patients with sphincter of Oddi dysfunction suitable for treatment with EPT.

Adult↗

Frequency of biliary crystals in patients with suspected sphincter of Oddi dysfunction.

BACKGROUND: The passage of gallstones (macro- or microlithiasis) is theorized to play a role in inducing sphincter of Oddi dysfunction. This study examined the frequency at which biliary crystals are found in patients with suspected type II and type III sphincter of Oddi dysfunction. METHODS: A total of 85 patients (66 women, 19 men; mean age 38 years) with unexplained abdominal pain of suspected pancreatobiliary origin and no prior episode of pancreatitis underwent ERCP with sphincter of Oddi manometry and bile collection for crystal analysis. Eighty-one patients had a gallbladder in situ. No patient had evidence of stones or sludge on prior abdominal imaging. Sphincter of Oddi manometry was performed in standard retrograde fashion by using an aspirating catheter. Patients were classified by sphincter of Oddi dysfunction type by using a modified Hogan-Geenen classification system. Patients with type I sphincter of Oddi dysfunction were excluded. Bile was collected directly from the gallbladder (n=23) or common bile duct (n=62) after an infusion of 3.5 microg of cholecystokinin and was examined by light and polarizing microscopy for cholesterol crystals or calcium bilirubinate granules. RESULTS: The proportion of patients with crystals was 3.5% (3/85). Thirty-five patients (41%) had elevated biliary and/or pancreatic sphincter pressure (type II, 16; type III, 19), of whom one (3%) had cholesterol crystals. Fifty patients had normal sphincter pressure, of whom two (4%) had cholesterol crystals (p=0.6). All 3 patients with cholesterol crystals had a gallbladder in situ. Calcium bilirubinate granules were not found in any patient. CONCLUSIONS: Microlithiasis appears to be rare in patients suspected to have type II or type III sphincter of Oddi dysfunction. Evaluation of bile for crystals appears unproductive in this group of patients.

Adolescent↗

Correlation between sphincter of Oddi manometry and intraductal ultrasound morphology in patients with suspected sphincter of Oddi dysfunction.

BACKGROUND AND STUDY AIMS: Intraductal ultrasonography (IDUS) makes it possible to study sphincter of Oddi morphology during endoscopy. Two recent IDUS studies have described the sphincter of Oddi as a circumferential hypoechoic layer in the papilla, but there have as yet been few published data from patients with suspected sphincter of Oddi pathology. PATIENTS AND METHODS: Twenty-one consecutive patients with suspected biliary sphincter of Oddi dysfunction (seven men, 14 women; age 54 +/- 17 years) were enrolled in the study. Endoscopic sphincter of Oddi manometry was carried out using a 4-Fr electronic microtransducer device. After this, a wire-guided 6-Fr ultrasound catheter was placed in the common bile duct (CBD), and IDUS was carried out while the ultrasound catheter was being withdrawn from the CBD toward the duodenum. RESULTS: Sphincter of Oddi manometry and IDUS were carried out successfully in 18 of the 21 patients. Sphincter of Oddi manometry revealed sphincter of Oddi hypertension (baseline pressure > 35 mmHg) in eight patients. The mean sphincter of Oddi baseline pressure was 32 +/- 17 mmHg, and the mean phasic sphincter of Oddi pressure was 132 +/- 31 mmHg. During IDUS, a circumferential hypoechoic layer was clearly delineated in all patients. There was a significant correlation between the manometrically determined length of the sphincter of Oddi (8 +/- 2 mm) and the thickness of the hypoechoic layer (6 +/- 2 mm) as assessed by IDUS (r = 0.66, P < 0.001). However, no correlation was found between the baseline or phasic sphincter of Oddi pressures and the thickness of the hypoechoic layer. Accordingly, IDUS did not allow identification of patients with sphincter of Oddi hypertension. Mild pancreatitis was observed in one of the 18 patients (6 %). CONCLUSIONS: The circumferential hypoechoic layer of the papilla visualized by IDUS is the ultrasonographic correlate of the sphincter of Oddi. IDUS of the papilla is technically feasible and safe in patients with suspected sphincter of Oddi dysfunction. IDUS may provide additional information at the sphincter of Oddi level, but cannot be used as a substitute for sphincter of Oddi manometry.

Adult↗

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 less than 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.

Adult↗

Sphincter of Oddi dysfunction.

Biliary-like pain alone, or associated with a transient increase in liver or pancreatic enzyme, may be the clinical manifestations of sphincter of Oddi dysfunction. Since it is not always possible to dissociate functional conditions from subtle structural changes, the term sphincter of Oddi dysfunction is used to define motility abnormalities caused by 'sphincter of Oddi stenosis' and 'sphincter of Oddi dyskinesia'. Both sphincter of Oddi stenosis and sphincter of Oddi dyskinesia may account for obstruction to flow through the sphincter of Oddi and may thus induce retention of bile in the biliary tree and pancreatic juice in the pancreatic duct. Most of the clinical information concerning sphincter of Oddi dysfunction refers to post-cholecystectomy patients who have been arbitrarily classified according to clinical presentation, laboratory results and endoscopic retrograde cholangiopancreatography findings in: (a) biliary type I, (b) biliary type II, and (c) biliary type III. Prevalence of biliary-type of pain has been reported to vary from 1 to 1.5% in unselected postcholecystectomy people, to 14% in a selected group of patients complaining of postcholecystectomy symptoms. The frequency of sphincter of Oddi dysfunction, as shown by manometry, differs in the different clinical subgroups: 65-95% in biliary group I, mainly due to sphincter of Oddi stenosis; 50-63% in biliary type II, and 12-28% in biliary type III. In patients with idiopathic recurrent pancreatitis, sphincter of Oddi dysfunction varies from 39 to 90%. Diagnostic work-up of postcholecystectomy patients for suspected sphincter of Oddi dysfunction includes liver biochemistry and pancreatic enzymes, plus negative findings of structural abnormalities. Usually, this would include transabdominal ultrasound and endoscopic retrograde cholangiopancreatography. Depending on the available resources, endoscopic ultrasound and magnetic resonance cholangiography may precede endoscopic retrograde cholangiopancreatography in specific clinical conditions. Quantitative evaluation of bile transit from the hepatic hilum to the duodenum at choledochoscintigraphy appears valuable in the decision to undertake sphincter of Oddi manometry or to treat. Sphincterotomy is the standard treatment for sphincter of Oddi dysfunction. In biliary type I patients, the indication for endoscopic sphincterotomy is straightforward without the need of any additional investigation. Slow bile transit in biliary type II is an indication to undergo endoscopic sphincterotomy without sphincter of Oddi manometry. Slow bile transit in biliary type III patients is an indication to perform sphincter of Oddi manometry. Diagnostic work-up of patients with gallbladder in situ is part of the same diagnostic algorithm that has initially excluded the presence of a gallbladder dysfunction.

Constriction, Pathologic↗