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Although controversy has surrounded the existence and function of the sphincter of Oddi (SO) since its initial description by Rugero Oddi in 1887, animal studies, and to a lesser extent human studies, have subsequently confirmed its existence and clarified the important anatomic and physiologic functions of the sphincter [1]. The SO, located at the distal extremity of the bile and pancreatic ducts, is comprised of tonically active smooth muscle that controls the flow of bile and pancreatic juice into the second portion of the duodenum. During feeding, cholecystokinin (CCK) as well as other hormones and neurally mediated reflexes stimulate gallbladder contraction and pancreatic secretion as well as relax the SO. This coordinated activity enables bile and pancreatic secretions to enter the duodenal lumen in order to facilitate digestion and absorption [2]. Superimposed upon a SO basal pressure of 5–10 mmHg are phasic contractions of 100–150 mmHg. Since SO basal pressure is higher than duodenal basal pressure and phasic contractions of the SO are almost coincident with duodenal phasic contractions, the SO also prevents reflux of duodenal contents into the biliary and pancreatic ducts [3]. Over the past several decades, yet more controversy has embroiled this muscle: do abnormalities in SO function result in a clinical disorder? In particular, the SO has been implicated as a potential cause of post-cholecystectomy syndrome, i.e., recurrent symptoms of biliary pain that occur in 10–15 % of patients after cholecystectomy. SO dysfunction (SOD) has also been proposed as an etiology for idiopathic recurrent pancreatitis and biliary-like pain in patients with an intact gallbladder without cholelithiasis. The proposed mechanism is functional obstruction from increased sphincter pressure due to spasm, hypertrophy, or denervation [1]. In the 1970s, the advent of endoscopic retrograde cholangiopancreatography (ERCP) served as an impetus for the development of miniaturized manometry catheters that could be passed through the working channel of a sideviewing endoscope and inserted into the biliary or pancreatic tree. In the 1980s, observational studies in humans using low-compliance manometry systems with multi-lumen catheters described several abnormalities in patients with suspected SOD including elevated basal pressure, a paradoxical rise in basal pressure with CCK injection, increased frequency of contractions with opiates, and abnormal retrograde contractions [4]. In 1988, Hogan and Geenan proposed the Milwaukee criteria for SO dysfunction or dyskinesia [5]. A revised version of their classification system that relied upon the presence or absence of elevated transaminases and bile duct dilatation during pain episodes was widely adopted. Patients with type 1 SOD had biliary-type pain, transaminases greater than twice the upper limit of normal, and bile duct diameter [12 mm during painful episodes. Type 2 SOD was defined as biliary pain plus only one of the two other criteria required to diagnose type 1 SOD. Type 3 SOD comprised patients with unexplained biliary pain with normal liver enzymes and normal caliber bile duct [5]. Surgical or endoscopic disruption of the biliary SO was a logical next step to treat SOD. Indeed, a randomized double-blind sham-controlled trial did demonstrate that patients with suspected type 2 SOD and high basal manometric pressures had significant and lasting & Tilak Shah Tilak.Shah@va.gov

Management of Sphincter of Oddi Dysfunction: Teaching an Old SOD New Tricks?