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Daniel Mønsted Shabanzadeh
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Kegnæs, M.; Novovic, S.; Shabanzadeh, D.M. Dysfunction of Biliary Sphincter of Oddi. Encyclopedia. Available online: https://encyclopedia.pub/entry/48450 (accessed on 03 July 2024).
Kegnæs M, Novovic S, Shabanzadeh DM. Dysfunction of Biliary Sphincter of Oddi. Encyclopedia. Available at: https://encyclopedia.pub/entry/48450. Accessed July 03, 2024.
Kegnæs, Marina, Srdan Novovic, Daniel Mønsted Shabanzadeh. "Dysfunction of Biliary Sphincter of Oddi" Encyclopedia, https://encyclopedia.pub/entry/48450 (accessed July 03, 2024).
Kegnæs, M., Novovic, S., & Shabanzadeh, D.M. (2023, August 24). Dysfunction of Biliary Sphincter of Oddi. In Encyclopedia. https://encyclopedia.pub/entry/48450
Kegnæs, Marina, et al. "Dysfunction of Biliary Sphincter of Oddi." Encyclopedia. Web. 24 August, 2023.
Dysfunction of Biliary Sphincter of Oddi
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This entry is adapted from the peer-reviewed paper 10.3390/jcm12144802

Biliary Sphincter of Oddi dysfunction (SOD) is one of the main causes of post-cholecystectomy pain. Biliary SOD is classified into three types according to Milwaukee classification, based on clinical presentation as well as laboratory and/or imaging abnormalities. As a functional disorder, SOD is classified according to Rome IV criteria. Currently, patients with post-cholecystectomy pain and SOD are mostly diagnosed by the Rome IV criteria. The management of SOD most often involves non-pharmacologic treatment, and high-level evidence supports sphincterotomy in type 1 and 2 SOD. Emerging high-quality data show no effect of sphincterotomy for patients with type 3 SOD. However, ERCP with biliary sphincterotomy is associated with post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis rates from 10% to 15%.

cholecystectomy post-cholecystectomy pain sphincter of Oddi dysfunction (SOD) sphincterotomy cholescintigraphy

1. Introduction

Post-cholecystectomy pain refers to the subsequent development of recurrent episodes of abdominal pain in patients who have had cholecystectomy [1][2]. This pain occurs in 10–20% of post-cholecystectomy patients [3]. The etiologies of persistent and incident symptoms after cholecystectomy and the underlying mechanisms could be different [4]. Common biliary causes include retained or recurrent common duct stones, fibrosis due to chronic inflammation of the bile duct, or, less commonly, an inflamed cystic duct remnant [5][6]. Sphincter of Oddi dysfunction (SOD) is another important cause of post-cholecystectomy pain that is defined as an abnormality of either the biliary and/or pancreatic sphincter causing intermittent or fixed obstruction to the flow of bile or pancreatic juice, associated with episodes of biliary-type pain, recurrent pancreatitis, elevated liver enzymes, or ductal dilatation [6][7][8][9][10]. Among those 10–20% of patients undergoing cholecystectomy who experience post-cholecystectomy biliary pain, 9–51% meet the diagnostic criteria for SOD [3][11]. Overall, patients with previous cholecystectomy are predisposed to SOD [11][12] and about 1.5% of patients develop SOD after cholecystectomy [13][14][15].

2. Anatomy and Pathophysiology

The Sphincter of Oddi (SO) is regulating the flow of biliary and pancreatic secretion into the duodenum [14]. The SO is a complex muscular structure that surrounds the intraduodenal segment of the common bile duct, the pancreatic duct and major duodenal papilla, and functions independently of the duodenal musculature [16][17]. Italian anatomist, Ruggero Oddi, initially described the SO in 1887 [14]. A clinical syndrome that is defined as an abnormality of either the biliary and/or pancreatic sphincter related to the intermittent or fixed obstruction to the flow of bile or pancreatic juice is defined as SOD [8][9]. The physiology of the SO is quite complex [18]. SOD includes both mechanical and functional component. SO stenosis is an anatomic (mechanical) abnormality related to the narrowing of the SO or its obstruction, that could result from any process causing inflammation or scarring (pancreatitis, gallstone passage, infection, malignancy) [16]. SO dyskinesia is related to a functional disturbance in muscular tone control causing an intermittent biliary obstruction.
Basal pressure of the SO is 10 mmHg in humans. Superimposed anterograde phasic contractions, initiated at the junction of the common bile duct (CBD) and the SO and progressing into the duodenum, occur in response to physiologic and exogenous stimuli and result in the evacuation of contents already present within the SO into the duodenum. During contraction, no additional flow from the CBD into the SO occurs. The SO then relaxes, allowing for the passive refilling of bile into the SO segment. Once filled, another wave of phasic contractions begins. When basal pressure increases, resistance to flow increases, resulting in gallbladder filling and the prevention of flow into the duodenum. When basal pressure decreases below CBD and pancreatic duct (PD) pressures, flow into the duodenum occurs [14].
The motility of the SO during the digestive period involves both neural and hormonal input [18][19][20][21][22]. In this period, there are gallbladder contractions, stimulation of pancreatic secretion, and SO relaxation, leading to high rates of bile and pancreatic secretion into the duodenum. Cholecystokinin (CCK) is the most important hormone involved in SO motility. CCK decreases SO basal pressures and inhibits phasic contractions, thereby promoting anterograde flow. Enteroendocrine cells of pancreas secrete CCK in response to a meal, leading to gallbladder contraction, the relaxation of SO and the secretion of pancreatic enzymes, via both direct action on CCK receptors and indirect action through cholinergic neurons [14]. After cholecystectomy, the normal biliary tree is transformed into a single-outlet system in which intrahepatic ductal bile flows only through the bile duct into the duodenum [17]. Moreover, the biliary system no longer has a pressure-release mechanism, formerly served by gallbladder. If the SO resists flow, increased pressure produces pain [1] and may lead to biliary stasis and ductal dilation [17].
Thus, gallbladder function appears to play a critical role in SO mechanics; therefore, patients, after cholecystectomy, are more likely to develop SOD. It is also shown that, in patients with an intact gallbladder, CCK inhibits the SO phasic wave activity, but 6 months after cholecystectomy, CCK fails to inhibit this activity [11][23]. Furthermore, it is demonstrated that patients with post-cholecystectomy pain had elevated basal SO pressure, retrograde phasic wave contraction, and an increase in phasic wave frequency greater than seven contractions per minute. However, it is still unclear whether post cholecystectomy patients develop SOD due to elevated basal pressure, altered motility of the SO, or both [11][14].

3. Clinical Manifestations, Classifications, and Laboratory Findings

Episodes of biliary pain are one of the most common manifestations of SOD, as well as recurrent pancreatitis, elevated liver enzymes, or ductal dilatation. Symptoms of biliary pain ascribed to gallstones have traditionally been termed “biliary colic” and were originally defined by a sudden debut of intense and agonizing pain, localized in the right hypochondrium or epigastrium, with projection to the shoulder, and a duration ranging from hours to weeks. Later, more simple definitions of biliary pain were formulated in gallstone screening studies including abdominal pain during the last five years, with a duration of more than 30 min, and with localization in the right hypochondrium and/or epigastrium [7]. Biliary SOD is characterized by intermittent or episodic right upper quadrant pain that might not necessarily be postprandial and is often accompanied by nausea and vomiting. Based on these criteria, a few classifications of SOD have been developed over time.
As a structural abnormality, biliary SOD is classified according to Milwaukee classification into types 1, 2 and 3 based on clinical presentation as well as laboratory and/or imaging abnormalities [8][11][12][14][24][25][26][27][28]. Diagnosis of type 3 SOD is challenging due to the lack of significant abnormalities on laboratory testing or diagnostic imaging.
As a functional disorder, SOD is classified according to Rome IV criteria that are linked closer to clinical practice, based mainly upon expert consensus [14][16][29].

4. Diagnostic Challenges

In patients with previous cholecystectomy, the Rome IV consensus conference statement suggests that the reasonable approach towards the diagnosis of biliary SOD is to start with liver and pancreatic biochemical tests, followed by an upper endoscopy and abdominal imaging such as transabdominal ultrasound (US), computed tomography (CT) scan, magnetic resonance cholangiopancreatography (MRCP) or endoscopic ultrasound (EUS).
Previously, an elevation of basal sphincter pressure detected on endoscopic Sphincter of Oddi manometry (SOM) was the gold standard for establishing SOD diagnosis [2][5][30][31]. SOM is performed during ERCP and is the only investigation that can directly assess SO motor activity [32][33]. However, this method has mostly been abandoned, as it is an invasive procedure with a high risk of severe complications, such as post-ERCP pancreatitis rates of up to 30% [8][10][14][16][29][31][32][34][35][36][37]. Additionally, SOM is not a widely available technique due to the need for expertise to correctly perform and interpret the obtained manometric results [33][38].
The use of less invasive diagnostic methods for SOD is needed in order to replace the manometry measurements. Several new diagnostic modalities, such as functional Magnetic Resonance Imaging (functional MRI), Optical Coherence Tomography (OCT) and Functional Lumen Imaging Probe (FLIP) technique, have emerged in recent years [10][31][38][39].
Functional MRI is a class of imaging methods that is quite popular due to its wide availability, non-invasive nature, relatively low cost and good resolution. The visualization of the biliary tract is possible using gadolinium-based contrast agents that are taken up by normal hepatocytes and partially excreted in the biliary system [40]. Functional MRI is similar to hepatobiliary scintigraphy, but with a higher resolution, and the hypothesis that SOD is caused by the delayed emptying of a biliary excreted contrast agent to the duodenum is investigated [31].
Optical coherence tomography permits the high-resolution, real-time imaging of the SO microstructure by a probe inserted into the common bile duct through an ERCP catheter [39]. OCT uses low-power infrared light in order to highlight the details of the microstructure of the gastrointestinal wall layer in real time, and it allows for a much higher resolution with a much lower depth penetration compared to US. The intermediate layer of the papillary region in patients with type 1 SOD was 2.3 times thicker than that in control patients and its infrared light back-scattering showed the hyper-reflectivity of the fibromuscular layer of SO as compared to controls [31][39]. The FLIP technique is used to analyze the sphincter profile and motility patterns of the sphincter during ERCP. Botox injections temporarily interfere with SO motility, causing its relaxation and, in some cases, pain relief [10].
Hepatobiliary scintigraphy (cholescintigraphy) is a promising diagnostic imaging tool that has found broad clinical application. It is quantitative, reliable, and non-invasive method for diagnosing SOD in patients who have had cholecystectomy, although the clinical value of this modality is not well established. Hepatobiliary scintigraphy involves the intravenous injection of 99mTc-radioisotope compounds that are bound to serum albumin in the blood stream, which are dissociated from albumin in the hepatic presinusoidal space and extracted by hepatocytes by receptor-mediated endocytosis, similar to bile salts, free fatty acids and bilirubin. Afterwards, they follow the same metabolic pathway as bilirubin, except that they are secreted into biliary caliculi unchanged, without undergoing conjugation [1][16]. The time–activity curves for the radionucleotide excretion throughout the hepatobiliary system are measured [1][13][18][32][38][41]. This technique is used to assess the rate of bile flow into the duodenum. The literature regarding cholescintigraphy is relatively limited and quite challenging to interpret due to variations in methodology, clinical indications, categories of patients, time to peak activity, hepatic clearance at predefined time intervals, and a lack of consensus on its diagnostic use [1][10][16][17][18][32][38][41]. 

5. Treatment Options

5.1. Non-Pharmacologic Treatment

The management of SOD most often involves non-pharmacologic treatments such as ERCP and sphincterotomy [10][14], and the correlation between type of SOD and clinical outcome after biliary sphincterotomy is continuously being explored [8]. Endoscopic sphincterotomy is the most commonly used non-pharmacologic treatment for SOD for patients with type 1 and 2 SOD [10].
Two randomized controlled trials [2][42], including a sphincterotomy group and a control group receiving sham intervention, showed that patients with abnormally elevated basal pressure showed over 90% long-term relief in symptoms related to biliary-type pain when undergoing sphincterotomy of the biliary SO [43].

5.2. Pharmacologic Treatment

Calcium-channel blockers (nifedipine, nicardipine) are known smooth muscle relaxants that potentially could decrease the basal pressure of the SO [44][45]. Nifedipine has been explored in the SOD treatment in the randomized controlled trial [44] including 28 patients with elevated SO basal pressure without abnormal phasic wave contractions on SOM. Patients were treated with nifedipine or placebo over 12 weeks, with a subsequent cross-over. To monitor the level of biliary pain, patients kept diaries of pain levels and visits to the emergency department were registered. Compared with patients in the placebo group, patients in the nifedipine group had a significantly lower number of pain episodes and emergency room visits, and a decreased use of analgesics. Among all patients, 21 reported an improved pain level. Moreover, no significant differences in the tolerated nifedipine dose between groups were reported. However, patients with improved pain levels had predominantly antegrade propagation of phasic contractions, whereas patients who maintained their pain level had predominantly retrograde contractions. Thus, nifedipine decreased basal and phasic pressures, but did not have an effect on the sequence of phasic contractions [44].

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