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The Postcholecystectomy Syndrome: a Review of Etiology and Current

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The Postcholecystectomy Syndrome: a Review of Etiology and Current Gastroenterology Insights 2012; volume 4:e1 The postcholecystectomy bowel syndrome, chronic pancreatitis, and malignancy.5,7 Lasson et al. followed 65 Correspondence: Qiang Cai, Division of Digestive syndrome: a review patients initially diagnosed with PCS and Diseases, Emory University School of Medicine, of etiology and current found 48% with identifiable extrabiliary dis- 1365 Clifton Road, B1262 Atlanta, GA 30322, USA. approaches to management eases during 4-13 years of follow up.8 Similarly, Tel: +1.404.778.4857 - Fax: +1.404.778.2578. Filip et al. found 27 of 80 patients (34%) eval- E-mail: [email protected] uated for PCS actually had non-biliary symp- Robert D. Kung, Amanda W. Cai, Key words: postcholecystectomy syndrome, chole- 9 Jason M. Brown, Anthony M. Gamboa, toms. Others cite gastroparesis, costchondri- cystectomy, etiology. Qiang Cai tis, fibromyalgia, and chronic narcotic use as common causes for PCS pain.10 Thus, the first Received for publication: 9 June 2011. Division of Digestive Diseases, Emory step in evaluating patients with PCS must be a Accepted for publication: 29 August 2011. University, School of Medicine, Atlanta, careful history and evaluation to exclude these GA, USA This work is licensed under a Creative Commons common and often treatable disorders. Given Attribution NonCommercial 3.0 License (CC BY- the number of non-organic pain disorders NC 3.0). included in the differential, referral to a pain specialist may also be appropriate. ©Copyright Robert D. Kung et al., 2012 Abstract Licensee PAGEPress, Italy Organic biliary etiology Gastroenterology Insights 2012; 4:e1 Postcholecystectomy syndrome (PCS) com- doi:10.4081/gi.2012.e1 New biliary disorders may develop after prises a heterogeneous group of symptoms and cholecystectomy, and these must be ruled out disorders in patients who have previously through standard laboratory and radiological undergone cholecystectomy. While it is rela- assessments. Common bile duct stones and of Oddi dyskinesia, referring to a functional tively uncommon, it is defined by chronic cholangiocarcinoma can arise independently abnormality of the sphincter leading to inter- recurring pain, often with no clear source. of cholecystectomy. Obstructive symptoms mittent obstruction, perhaps due to still Recent studies suggest its pathogenesis require relief of the obstruction with prompt unknownonly neuro-hormonal disturbances.13 depends on different factors, but it remains endoscope retrograde cholangiopancreatogra- Stenosis is thought to occur in type 1 SOD, poorly understood and complex to treat. Here, phy (ERCP) or surgical intervention. inferred from its predictable response to we present a brief overview of this syndrome, Malignancy is associated with older age and sphincterotomy, whereas dyskinesia is thought review recent literature regarding its etiology, later presentation. Filip et al. recentlyuse pub- to occur in type 2 and type 3 SOD, which are and present a systematic approach to diagno- lished a cohort study demonstrating endoscop- less understood. sis and management. ic ultrasound was 96.2% sensitive and 88.9% Geenan and Hogan were the first to demon- specific for identifying pancreaticobiliary dis- strate relief of pain after endoscopic biliary eases.9 This approach helped define which sphincterotomy (EBS) in 91% (10 of 11) of patients warranted subsequent ERCP, reducing cholecystectomized patients with elevated Introduction both the number of ERCPs by 51% and the pro- sphincter of Oddi (SO) pressures at 12-month cedure related morbidity associated with this follow up, but no benefit in patients with nor- Cholecystectomy is one of the most com- procedure. Surgically related complications mal sphincter pressures.14 By contrast, two monly performed surgical procedures and is such as strictures and bile duct injuries have recent studies have found only 18-43% of the standard of care in treating symptomatic been described extensively elsewhere and are patients with definite SOD (i.e. proven by 1-4 gallstones. Up to a third of patients undergo- not the focus of this review.11 SOM) had complete resolution of symptoms at ing cholecystectomy will develop recurrent and 12-18 months after EBS.14-15 This suggests a persistent abdominal pain weeks to years after Functional biliary etiology: true pathogenesis which is more complex than 5-6 surgery. In the majority of patients, symp- postcholecystectomy syndrome sphincter dysmotility alone. Several studies toms are mild and short lived, but 2-5% will have implicated the development of visceral continue to have frequent debilitating pain, a Sphincter of Oddi dysfunction hyperalgesia and somatosensory hypersensi- condition referred to as the postcholecystecto-Non-commercialWhen basic evaluation has ruled out both tivity as a source of PCS which has been over- my syndrome (PCS).5 Rather than being a sin- extrabiliary disorders and gross biliary looked. Desautels et al. reproduced pain symp- gle disorder, this term encompasses a widely obstruction, sphincter of Oddi dysfunction toms in type III SOD patients by distending the varying group of disorders, including extrabil- (SOD) is believed to be the most frequently duodenum.16 Kuruscai et al. demonstrated iary, organic biliary, and functional biliary dis- identifiable cause of PCS. While the estimated increased hypersensitivity of peripheral noci- eases, considered true PCS (Table 1). In many incidence is less than 1% of all cholecystec- ceptive nerve fibers in the right upper quad- cases, no source of PCS can be identified, and tomized patients, SOD may account for 14% of rant of the abdomen. Less electrical stimuli symptoms remain unexplained and challeng- pain from PCS.12 Despite the prominence of were needed to illicit sensation in SOD ing to treat. This article is a review of the SOD in the differential diagnosis of PCS, the patients when compared to asymptomatic recent literature regarding the different etiolo- pathogenesis of SOD remains poorly under- cholecystectomized patients, symptomatic gies of PCS, and current diagnostic and thera- stood. Two mechanisms have been proposed: non-SOD patients, and healthy volunteers. It is peutic approaches to its management. sphincter of Oddi stenosis refers to a structur- thought that both peripheral nerve fibers and al abnormality resulting from inflammation central nerve fibers at the level of the spine are Extrabiliary etiology and scarring of the sphincter. Sphincter of hypersensitized, lowering the pain threshold, The most common causes of PCS may be Oddi basal pressures, which can be measured similar to the pathogenesis of other functional extrabiliary diseases, an umbrella classifica- by manometry (SOM) during ERCP, tend to be pain disorders, such as irritable bowel syn- tion including gastroesophageal reflux dis- above 40 mmHg, and do not change after phar- drome.17 Pain associated with injection of con- ease, gastritis, peptic ulcer disease, irritable macological challenge. The second is sphincter trast or saline during ERCP has been common- [Gastroenterology Insights 2012; 4:e1] [page 1] Review ly reported, but its significance is unknown.18 ical biliary pain follows the Rome III consensus ty of 100%.28,31-33 However, later studies found Linder et al. quantitatively measured symptom criteria for diagnosing functional biliary pain, only a 13% sensitivity despite 95% specifici- improvement in patients with proven SOD who although further studies are needed to prove its ty.34,35 These disparate results have raised ques- underwent EBS compared to those with sus- utility in managing these patients.29 Other tions regarding the reproducibility of scinti- pected SOD with normal SOM.19 At 18-months mechanisms such as visceral hyperalgesia are graphic results. The addition of morphine provo- follow-up, the SOD/EBS group was more likely more likely to be playing a role in this group of cation appeared to increase the sensitivity to to express symptom improvement, but both PCS patients, many of whom are likely misla- 83%, and was associated with 81% specificity.36 groups almost uniformly continued to experi- beled as having SOD.16 Many recent trials have studied how well ence pain, consistent with chronic pain disor- Given the potential morbidity, cost, and lack of secretin-stimulated magnetic resonance cholan- ders and suggesting a multifactorial etiology. availability of SOM, non-invasive strategies to giopancreatography (ss-MRCP) predicts the SOD has been historically classified into 3 evaluate SOD are needed. The morphine- results of SOM. It is to be noted that these stud- types according to the modified Milwaukee prostigmin test (Nardi test) was one of the ear- ies included patients with biliary and pancreatic Criteria, based on the presence or absence of 3 liest methods developed, but has very low sensi- type pain, idiopathic pancreatitis, as well those criteria: biliary type abdominal pain; elevation of tivity and specificity for predicting the presence with and without prior cholecystectomy. serum transaminases, alkaline phosphatase, or of SOD.30 Initial studies demonstrated that Prolonged increase in pancreatic duct diameter bilirubin to 1.5 times the upper limit of normal quantitative hepatobiliary scintigraphy (QHBS), after injection of secretin, which relaxes the SO, with normalization between attacks; and bile measuring the hepatic hilum to duodenal transit had previously been shown to correlate well with duct dilatation of more than 12 mm on imag- time of radio-labeled tracer, correlated well with ERCP diagnosis
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