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Sphincter of Oddi Dysfunction

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Sphincter of Oddi Dysfunction Sphincter of Oddi Dysfunction a b, Aaron J. Small, MD, MSCE , Richard A. Kozarek, MD * KEYWORDS Sphincter of Oddi dysfunction Biliary Pancreatic Sphincterotomy Endoscopic therapy EPISOD trial Patient selection KEY POINTS Sphincter of Oddi dysfunction (SOD) is a benign, acalculous disease that can result in biliary or pancreatic obstructive symptoms. Chronic, unrelenting epigastric or right upper quadrant pain is not caused by SOD. It is difficult, if not impossible, to diagnose SOD in patients with an intact gallbladder. Modified Milwaukee classification is the most relevant classification system in clinical practice. The classification and response to sphincterotomy of biliary SOD I to III has been defined by randomized controlled trials, whereas pancreatic SOD classification has not. Initial evaluation starts with history taking, biochemistries, and noninvasive imaging before proceeding with endoscopic retrograde cholangiopancreatography (ERCP) and sphincter of Oddi manometry, if necessary. Response to sphincterotomy depends largely on the type of disease, with excellent response to type I and variable results with type II. Recent level I evidence suggests no role for therapeutic ERCP for type III SOD, which has no better response to treatment than a sham sphincterotomy. INTRODUCTION Biliary dyskinesia has been known by a number of pseudonyms, including but not limited to ampullary spasm, papillary stenosis, and sphincter of Oddi dysfunction (SOD). The latter name disregards Glisson’s 1681 description of the bit of muscle Disclosure statement: Dr A.J. Small has no conflicts of interest or financial ties to disclose; Dr R.A. Kozarek (Virginia Mason Medical Center) received support from the National Institutes of Health (DK074739-07) as one of the investigators in the EPISOD Study. a Division of Gastroenterology, Digestive Disease Institute, Virginia Mason Medical Center, 1100 Ninth Avenue, Seattle, WA 98101, USA; b Division of Gastroenterology, Digestive Disease Institute, Virginia Mason Medical Center, University of Washington, 1100 Ninth Avenue, Seattle, WA 98101, USA * Corresponding author. E-mail address: [email protected] Gastrointest Endoscopy Clin N Am 25 (2015) 749–763 http://dx.doi.org/10.1016/j.giec.2015.06.009 giendo.theclinics.com 1052-5157/15/$ – see front matter Ó 2015 Elsevier Inc. All rights reserved. 750 Small & Kozarek encompassing the distal bile duct and credits Ruggero Oddi, a fourth year medical student at the University of Perugia, Italy, with its description in 1887 and its consequent dysfunction.1 What neither Glisson nor Oddi envisioned, however, was the controversy surrounding a 6- to 15-mm fragment of smooth muscle that Boyden has divided into three distinct histologic segments to include the sphincter ampullae.2 Like a theologic trinity, Oddi’s sphincter, therefore, has evolved into three. Clinical signs and symptoms accordingly are predicated on which of the subsphincters becomes inflamed, irritated, spastic, patulous, or hormonally belligerent.3 The senior author first wrote this more than 20 years ago.3 What has happened in the subsequent 2 decades that has made the authors rethink their approach to possible sphincter dysfunction? The entire paradigm of SOD may currently be unraveling with the questionable utility of effective endoscopic therapies for certain subtypes of SOD. The decision to perform endoscopic retrograde cholangiopancreatography (ERCP) with sphincterotomy for SOD is complex and involves several factors, such as patient characteristics, classifica- tion of the disease, local expertise, and potential predictors of response to therapy. When considering therapy for SOD, it is essential to partake in shared decision making with patients and consider each of these variables in order to develop the best approach for each patient having symptoms potentially attributable to the pancreaticobiliary sphincters. This article reviews the current definition of SOD and the various factors to consider before embarking on endoscopic therapy for SOD in light of recent evidence. DEFINING SPHINCTER OF ODDI DYSFUNCTION The sphincter of Oddi (SO) serves as the dynamic gatekeeper for pancreaticobiliary endoscopists as a cylindrical anatomic structure composed of 3 sphincters of smooth muscle fibers that surround the distal common bile duct (CBD), main pancreatic duct, and the ampulla of Vater (Fig. 1).4–6 Given its anatomic position surrounding the intra- mural portion of the CBD and pancreatic ducts, SO contractility directly regulates the (antegrade) flow of bile and pancreatic juices out into the duodenum and prevents (retrograde) reflux of duodenal fluid into the pancreaticobiliary tree. Dysregulation of SO contractility, involving either of the biliary or pancreatic portions of the sphincter or both, can result in an impedance of flow, alleged to be responsible for biliary colic as well as a source for acute, relapsing pancreatitis. Inflammation and fibrosis at the papillary orifice may also contribute to sphincter spasm or stenosis.7 The resultant clinical syndrome of this dyskinetic or stenotic sphincter is characterized as SOD. Diagnosis is often made after excluding overt stone disease and other structural causes for pancreatic or biliary pain, including ductal stenosis or stones. A variety of other terms, including papillary stenosis, sclerosing papillitis, biliary spasms, biliary dyskinesia, and postcholecystectomy pain syndrome, have been linked to SOD, further adding to the confusion of this disease. SOD remains a controversial clinical entity that is multifactorial and may present with complex symptoms. Pathogenesis The cause of SOD is not well understood. It is categorized as a benign, acalculous obstructive disorder at the level of the SO.8 There are several proposed causes. One is the formation of a stenosis at the ampulla from passage of a gallstone or gravel over an extended time period. A second possibility is attributed to SO hypertension either caused by a congenital hypertrophic sphincter or an overly responsive smooth muscle contraction of the sphincter to neuronal or hormonal stimuli. Sphincter of Oddi Dysfunction 751 Fig. 1. SO anatomy. (From Elmunzer BJ, Elta GH. Biliary tract motor function and dysfunc- tion. In: Feldman M, Friedman LS, Brandt LJ, editors. Sleisenger and Fordtran’s gastrointes- tinal and liver disease: pathophysiology/diagnosis/management. 9th edition. (PA): Saunders Elsevier; 2010. p. 1068; with permission.) Epidemiology The prevalence of SOD is difficult to ascertain given that the diagnosis is one of exclu- sion and based on a high level of suspicion, often after response to a biliary and/or pancreatic sphincterotomy. Up to 1.5% of the US population report symptoms consis- tent with SOD based on survey data, with a 3-fold female predilection.9 It is estimated that 10% to 20% of patients who undergo cholecystectomy have subsequent recur- rent or residual upper abdominal pain; these patients may have SOD.10–13 Estimates for pancreatic SOD are limited to small cohort studies with 33% to 40% of idiopathic recurrent pancreatitis suspected to be from SOD.14 Classification of Sphincter of Oddi There have been several reported classification schemes of SOD in an effort to objectify the diagnosis. The most widely adopted is the Milwaukee classification scheme pro- posed by Hogan and Geenen.15 In this scheme, SOD is classified into biliary types I, II, and III based on upper abdominal symptoms, biochemical abnormalities, and radio- graphic results (Table 1).6,15 Subsequently, this classification was broadened to include patients with pancreatic-type pain and relapsing pancreatitis (by single-center expert opinion but never validated in randomized controlled trials [RCTs]). Type I is character- ized by (1) dilated CBD or main pancreatic ducts, with some variations in the cutoffs in what is considered a dilated duct (note that the classification fails to consider the degree of bile dilation before and after cholecystectomy); (2) greater than a 1.5- to 2.0-fold elevation in liver-associated enzymes (aminotransferases or alkaline phosphatase levels) or pancreatic enzymes (amylase or lipase) on at least 2 occasions during epi- sodes of pain; and (3) typical, episodic biliary, or pancreatic pain. Type II is suspected when 2 of the 3 aforementioned criteria are present. Finally, type III has been defined by 752 Small & Kozarek Table 1 Modified Milwaukee classification scheme Classification Diagnostic Criteria A. Biliary SOD Type 1 1. Biliary-type pain 2. Elevated ALT, AST, AP more than 1.5–2.0 times the upper limit of normal on at least 2 or more occasions 3.Bile duct diameter 10 mm Type 2 Biliary-type pain with either B or C in the aforementioned criteria Type 3 Biliary-type pain only with no other abnormalities B. Pancreatic SOD Type 1 1. Pancreatic-type pain 2. Elevated serum amylase or lipase more than 1.5–2.0 times the upper limit of normal on at least 2 or more occasions 3. Pancreatic duct diameter 6 mm in the head and 5 mm in the body Type 2 Pancreatic-type pain with either B or C in the aforementioned criteria Type 3 Pancreatic-type pain only with no other abnormalities Abbreviations: ALT, alanine aminotransferase; AP, alkaline phosphatase; AST, aspartate aminotransferase. intense biliary or pancreatic-type pain alone with no evidence of laboratory or radio- graphic abnormalities during episodes of pain or at baseline. Despite these criteria, some remain skeptical of the diagnosis, contending that type I is rather a consequence
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