Sphincter of Oddi Dysfunction

The case study by Hadique and colleagues describes a 36-year-old woman who presented with biliary colic, aminotransferase elevations at three times the normal levels, and a 10-mm bile duct on ultrasound and computed tomography (CT) examination.¹ There was no evidence of either gallstones or common bile duct stones, and a tentative diagnosis of sphincter of Oddi dysfunction (SOD) was made. Endoscopic retrograde cholangio-pancreatography (ERCP) revealed choledocholithiasis. Whether the patient underwent sphincterotomy, balloon dilation of the sphincter with stone extraction, periampullary botulinum toxin injection, or laparoscopic or open common bile duct exploration at the time of cholecystectomy was not reported.

There are clinical clues in a patient such as this that point to stones, spasm, or papillary stenosis as the etiology of the symptoms. A single episode of biliary colic, in conjunction with the elevation of liver function tests with or without hyperamylasemia or dilated biliary tree on imaging, signifies stone disease until proven otherwise. The authors do not specify the timing of ERCP relative to clinical presentation or whether the patient maintained symptoms and laboratory abnormalities prior to manipulation. This information is crucial, even before considering a diagnosis of SOD. Just as continuous, unrelenting epigastric or right upper quadrant pain is highly unlikely to be related to sphincter spasm or even stenosis, a single pain episode in this setting simply demonstrates that the diagnostic technology employed is imperfect. In fact, common bile duct stones are seen on ultrasound in only one half to two thirds of patients with choledocholithiasis and approximately one third of patients studied with CT.^2–4 Both endoscopic ultrasound (EUS) and magnetic resonance cholangiopancreatography (MRCP) would have confirmed the diagnosis in this patient, although their application is contingent upon the relative skill sets of surgeons and therapeutic endoscopists in an institu-tion.^2–5 In hospitals in which surgeons routinely perform transcystic laparoscopic common bile duct exploration, an EUS or MRCP would have resulted in a laparoscopic approach in this 36-year-old patient in whom unnecessary sphincter manipulation could potentially result in acute or possible long-term complications. In institutions without this expertise, ERCP can be both diagnostic and therapeutic for common bile duct stones, often reserving laparoscopic cholecystectomy for patients with concomitant gallstones or imaging evidence of concomitant gallbladder disease.^6–10

SOD is a multifactorial disease with complex symptoms. Purported to cause recurrent biliary colic, as well as acute and relapsing pancreatitis, SOD is diagnosed depending upon both definition of the disorder and, to some extent, geography.^11–13 For instance, many of our colleagues in Europe and Asia are skeptics of SOD, defining type I SOD (ie, dilated ducts, delayed drainage, 1.5–2-fold elevation in aminotransferase levels on at least 2 occasions in a patient with recurrent biliary colic) as simply a consequence of chronic gravel or sludge passage with subsequent papillary stenosis. Type II SOD (ie, intermittent pain plus either ductal dilation or liver function abnormalities, since delayed ductal drainage has recently been dropped as a diagnostic criterion) is purported to result from gravel passage without structural stenosis. Type III SOD (ie, intense pain) is a functional disorder that covers a spectrum of problems including gastroparesis, irritable bowel syndrome, nonulcer dyspepsia, and sphincter spasm.¹⁴ Moreover, previous studies have documented that these patients demonstrate visceral hyperalgesia and pain that reproduces the symptoms simply by balloon inflation in the duodenum.

Papers written by Sherman and Lehman,¹⁵ Baillie,¹³ and Petersen^16,17 have provided vital reviews of SOD. This commentary will synopsize only a few salient points.

1. Most patients do not fit within standard SOD cat-egories.¹⁴ For example, physicians may not be certain whether a patient with a 9-mm bile duct, pain, and aminotransferase elevations of 1.4 times the normal level should be classified as type I SOD, type II SOD, or neither. Likewise, it is unclear how a patient with a 15-mm common bile duct, periodic severe pain superimposed upon a background ache, but normal aminotransferase levels should be classified. Similarly, in a patient with an intact gallbladder and no imaging evidence of stones, recurrent biliary colic and 1.5-fold transaminase elevation could be a function of gravel passage or sphincter dysfunction. The diagnosis changes if the patient has a 10-mm or 3-mm common bile duct.

2. Although a variety of noninvasive studies have been advocated in the diagnosis of SOD, including morphine-prostigmin test, biliary scintigraphy transit studies, cholecystokinin ultrasound, secretin EUS or MRCP, and diagnostic trials of ampulla of Vater botulinum toxin injections, SOD manometry remains the gold standard of diagnosis.^{13,15,17–22}

3. Although moderated by the placement of small-caliber stents in the pancreatic duct (whether or not sphincter pressure is abnormal and whether or not a biliary, pancreatic, or dual sphincterotomy is performed), post-ERCP pancreatitis occurs at least 2–5 times more often in patients with SOD, as opposed to patients who undergo ERCP for choledocholithiasis.^15,22 Moreover, the sphincter is a dynamic structure, and our group, as well as others, has studied patients with vastly discordant sphincter pressures when undertaking SOD manometry on different days.

4. The main conundrum does not lie with type I SOD or even true type II patients, almost all of whom have their biliary sphincters ablated without undertaking manometry prior to their referral to a tertiary pancreaticobiliary referral center—it lies with the type III SOD patients with only pain, or pain plus aminotransferases or amylase elevated 10% on one or more occasion. These patients have a normal pancreaticobiliary tree on CT and MRCP, have often undergone a negative EUS or one that is interpreted as having several diagnostic criteria for chronic pancreatitis, and may or may not have an intact gallbladder. This latter patient group, previously defined by Cotton as the group that needs ERCP the least and the group most likely to be injured by it, has, at best, a 50% chance of pain improvement whether one ablates one sphincter or two.^{16,17,23–25} This finding suggests that our gold standard is, at best, a gilded one. Most surgeons do not remove gallbladders for chronic right upper quadrant pain unless there is imaging or scintigraphic evidence of stones or dyskinesia and pain reproduction with scintigraphy.^26,27 We, as endoscopists, have not developed that same level of discipline, and many patients are subjected to ERCP with little to recommend it other than the laments of the patients. This is particularly ironic as the risk of ERCP in this subgroup may be a log factor higher than an empiric cholecystectomy. Hopefully, an upcoming multicenter controlled trial investigating sphincterotomy versus sham-sphincterotomy for type III SOD patients will answer questions about the incidence of SOD in these patients, their psychological profile, the efficacy of single or dual sphincterotomy in the short term and long term, procedural complications, and their quality-of-life scores pretreatment and posttreatment.¹³ Until that time, diagnostic ERCP in these patients is best limited to pancreaticobiliary referral centers.