Gallbladder Dysfunction: How Much Longer Will It Be Controversial?

Gallbladder Ejection Fraction and Sphincter of Oddi Dysfunction in Acute Idiopathic and Acute Recurrent Pancreatitis in Children

The term “dysfunction” defines the motor disorders of the gall bladder and the sphincter of Oddi (SO) without note of the potential etiologic factors for the difficulty to differentiate purely...

Chronic acalculous gallbladder disease (CAGD) falls within the spectrum of diseases associated with gallbladder dysmotility. Cholecystokinin-cholescintigraphy (CCK-CS) has been used to evaluate for CAGD, with a gallbladder ejection fraction (GBEF) of <35% being indicative of gallbladder dysfunction. The reproduction of biliary colic upon administration of CCK has been cited as indicative of CAGD. Our purpose was to determine whether low GBEF or reproduction of pain during CCK-CS was predictor of surgical outcomes related to resolution of symptoms or as a correlate to gallbladder pathology. A retrospective review of patients was performed to evaluate adults with a diagnosis of CAGD who underwent CCK-CS prior to surgical intervention. CPT and ICD-9 coding queries were used to identify the patient population. Patients with cholelithiasis were excluded. Sixty-four patients met inclusion criteria. Two patients were lost to follow-up and were excluded. During CCK-CS, 41 patients (66%) reported symptoms similar to their presenting complaint. Twenty-one patients reported no symptoms with CCK-CS. There was no significant relationship between gallbladder pathology and either GBEF or reproduction of symptoms with CCK-CS (p=0.14). About 81% of patients (n=50) had relief of symptoms following cholecystectomy. Sixty-six percentage of patients (n=33) with long-term symptom relief after cholecystectomy had reproduction of symptoms with CCK-CS. Nineteen percentage of all patients (n=12) had long-term symptom recurrence despite surgery. Eight of these patients (66%) had symptom reproduction with CCK-CS. There was no significant correlation with either the GBEF or symptoms reproduction with CCK-CS as a predictor of postoperative outcome (p=0.12). Provocation of pain by CCK-CS and low GBEF are unreliable predictors of postoperative relief of symptoms following cholecystectomy for biliary dyskinesia or chronic acalculous gallbladder disease.

Gallbladder and biliary dyskinesia are conditions that are becoming increasingly recognized due to improved technology. They are motility disorders that affect the gallbladder and sphincter of Oddi (SO), respectively. Gallbladder dyskinesia presents with typical biliary pain in the absence of gallstones. Work-up includes laboratory tests and imaging to rule out gallstones. Further investigation leads to a functional radionuclide study to investigate gallbladder ejection fraction. An ejection fraction of less than 40% is considered abnormal, and patients should be referred for cholecystectomy. Symptom relief after the procedure has been seen in 94% to 98% of patients. The term sphincter of Oddi dysfunction (SOD) describes a collection of pain syndromes that are attributed to a motility disorder of the SO. SOD can be further subdivided into biliary and pancreatic SOD. Patients typically have had a prior cholecystectomy and present with episodic biliary pain. The initial work-up includes laboratory tests and imaging to rule out other structural causes of abdominal pain, such as retained gallstones. Imaging and laboratory studies further subdivide patients into types of SOD. SO manometry (SOM) is the gold standard for assessing biliary dyskinesia and can help stratify patients into one of two groups: SO stenosis versus SO dyskinesia. Those with stenosis (type I SOD) are the most likely to respond to treatment with endoscopic biliary sphincterotomy (EBS). As the vast majority of type I patients (>/= 90%) benefit from EBS, SOM is not necessary. Pancreatic SOD patients can be similarly divided into one of three groups. These patients present with recurrent bouts of abdominal pain and/or pancreatitis in the absence of gallstones or other structural abnormalities. Pancreatic sphincter manometry can help distinguish which patients would benefit from endoscopic pancreatic sphincterotomy. Recurrent stenosis of the opening after endoscopic treatment in these patients may necessitate a surgical (open) approach.

To evaluate the role of quantitative cholescintigraphy with fatty meal in the management of biliary dyskinesia and to describe the findings according to Sostre score (SS) criteria in patients with gallbladder (GB) in-situ and biliary pain. We performed a retrospective analysis of the hepatobiliary (HIDA) studies (n = 35) performed for evaluation of biliary dyskinesia either due to biliary pain, opioid induced sphincter of Oddi dysfunction (SOD), recurrent pancreatitis (RP) or post cholecystectomy syndrome (PCS). Gallbladder ejection fraction (GBEF) was calculated from the post fatty meal HIDA images (excluding PCS patients). Studies with GBEF ≤40 % and SS >4 were considered to have cholecystopathy and SOD respectively. Three of the 13 patients with PCS had SS of 6 each, suggestive of SOD. Delayed biliary visualization (>15 min) and activity in common bile duct 60 min > liver 15 min were the specific features in these cases. Opioid induced SOD patients had SS >4 with retrograde refilling of GB in one patient and normalization of the SS parameters after nifedipine challenge in the other patient. Patients with RP and biliary pain were stratified into four groups, normal (GBEF >40 % and SS ≤4), cholecystopathy (GBEF ≤40 % and SS ≤4), normal with SOD (GBEF >40 % and SS >4) and cholecystopathy with SOD (GBEF ≤40 % and SS >4). Four patients with intact GB had cholecystopathy with scintigraphic features of SOD. Quantitative cholescintigraphy with fatty meal and SS scoring identified biliary dyskinesia and SOD in patients with biliary pain, recurrent pancreatitis and post-cholecystectomy syndrome.

Use of laparoscopic cholecystectomy for biliary dyskinesia in the child

After successful antiviral treatment, most patients still have changes caused by the C virus: liver fibrosis, cryopathies, vasculitis, gallbladder and sphincter of Oddi dyskinesia, and lesions of other digestive organs. According to various authors, the most common residual changes are biliary motility disorders (30—85%). In most cases, such changes are not actively detected or corrected by the specialists who have treated these patients with antiviral therapy. Often, the treatment of such manifestations is limited to recommendations to change the way of eating and take antispasmodics ‘on demand’. One of the means for the effective treatment of these patients is the dietary supplement Holiver, which contains turmeric powder, artichoke extract, and medical bile extract Objective — to determine the frequency of gallbladder dysfunctions in patients after antiviral therapy for hepatitis C, as well as to assess the effectiveness of «Holiver». Materials and methods. A total of 163 patients (75 men, 88 women) aged 21—65 years with confirmed HCV elimination after antiviral treatment were examined. Gallbladder dysfunction was diagnosed in 55 patients (33.7%). Patients were randomized into two groups: group 1 (n=23) received standard therapy, group 2 (n=22) additionally received Holiver 2 tablets three times daily for 1 month, during the second month, they received only on‑demand antispasmodics for pain attacks (n=22). Clinical assessment was performed at baseline, 2 weeks, 1 and 2 months; laboratory and ultrasound evaluations were performed at baseline, 1 and 2 months. Results. In the group taking Holiver, a statistically significant decrease in the intensity of abdominal pain, bitterness in the mouth and flatulence (p&lt;0.05), as well as the need for antispasmodics, was recorded. There was a decrease in bilirubin levels, alkaline phosphatase activity, an increase in the gallbladder contraction index and a decrease in the frequency of sludge detection by ultrasound. The achieved positive effect was maintained one month after the completion of therapy. Conclusions. Gallbladder dysfunction is diagnosed in one‑third of patients after successful treatment of hepatitis C, mainly in the form of hypomotor dysfunction. The use of Holiver demonstrated efficacy and safety, significantly reducing clinical symptoms, improving laboratory parameters, and restoring gallbladder function.

Introduction: Biliary dyskinesia (BD) is diagnosed in patients who present with biliary colic, reduced ejection fraction of the gallbladder on a cholescintigraphy study (HIDA) scan and absence of gallstones on ultrasound. Laparoscopic cholecystectomy (LC) still remains the treatment of choice for biliary dyskinesia. Very few studies have looked at long-term response or efficacy of LC based on severity of gallbladder hypo function on a HIDA scan. Aim: To determine if long term symptom relief post LC in patients with BD or chronic acalculous cholecystitis is predicted by severity of gallbladder dysfunction. Methods: This was a retrospective study conducted at West Virginia university between 2005 and 2013. There were a total of 2,350 patients who underwent a cholecystectomy (either open or laparoscopic). Of these patients, 1,955 underwent LC, out of which 226 patients had the clinical diagnosis of chronic alcalculous cholecystitis. Data collection included demographics, pre operative patient symptoms, results of imaging studies, pathologic diagnosis and early post-operative pain relief. Our inclusion criteria was age >18, lack of gallstones on right upper quadrant ultrasound, normal liver function tests, diagnosis of BD determined by HIDA scan ejection fraction less than 35% and finally a pathology report confirming the diagnosis of chronic acalculous cholecystitis. Any pre operative or post operative workup was also reviewed. Long term symptom relief data was obtained via telephone interview using modified Likert scale. Based on this scale, patients were classified as either responder or non-responders. Results: A total of 209 patients met the above inclusion criteria. The mean long-term follow-up was 6.1 years. In 94 patients who had EF<10%, 86 were responders and 8 were non responders (response rate 92%, odds ratio [OR] 17.2; p-value<0.000). In 102 patients who had EF 10-35%, 68 patients were responders while 34 were non responders (response rate 67%, OR 3.2; p-value 0.056). The rest of the 13 patients were part of the reference group with gallbladder ejection fraction >35% who still ended up undergoing LC given ongoing biliary symptoms. All of the non responders in the <10% group either had pre or post operative testing that revealed alternative diagnosis. Conclusion: Severity of gallbladder dysfunction predicts long term response to laparoscopic cholecystectomy in patients with gallbladder dysfunction. Further studies with a larger group of patients should be done to corroborate our study results.

Chapter 106 - Biliary Dyskinesia and Sphincter of Oddi Dysfunction

Sphincter of Oddi dysfunction (SOD) refers to structural alterations (stenosis) or functional abnormalities (dyskinesia) of the sphincter of Oddi that can impede biliary and pancreatic duct flow, causing recurrent upper abdominal pain with or without abnormalities of liver or pancreatic chemistries or dilated duct. SOD is divided into two clinical entities, biliary SOD and pancreatic SOD. Typically, patients with SOD have symptoms such as recurrent attacks of the epigastrium and/or right upper quadrant pain or idiopathic recurrent acute pancreatitis. The diagnosis may be supported by hepatobiliary scintigraphy or provocation tests such as secretin MRCP but definitive diagnosis requires sphincter of Oddi manometry (SOM). Patients with type I biliary SOD who have biliary-type pain, abnormal liver tests, and a dilated common bile duct are referred for endoscopic sphincterotomy (EST) without manometry. Patients with type II biliary SOD who have biliary-type pain and either abnormal liver tests or a dilated common bile duct are referred for SOM and that an EST be performed if there is evidence of sphincter of Oddi stenosis. Patients with type III biliary SOD who have only biliary-type pain should avoid undergo ERCP and EST due to higher risk of complications and no benefit from EST. Patients with pancreatic SOD present with recurrent episodes of pancreatitis and have a negative evaluation for alternate causes. Patients who have suspected pancreatic SOD will typically require SOM and that those with elevated sphincter pressures undergo EST.

Sphincter of Oddi dysfunction (SOD) is a poorly-understood disorder, typically presenting as postcholecystectomy, "biliary-type," right-sided abdominal and/or chest wall pain. Most patients referred to specialist clinics for work-up of presumed SOD do not, in fact, have anything wrong with their bile ducts or biliary sphincter mechanisms. A careful history and focused physical examination will often identify the true source of the pain syndrome, ranging from chest wall costochondritis and nerve injury at surgical trochar sites, to gastroparesis and visceral hypersensitivity ("irritable bowel"). The Rome III classification of functional gallbladder and biliary disorders defines SOD as episodic (not daily) pain lasting more than 30 min, which is disruptive of normal activities and not associated with bowel upset. It is not relieved by gastric acid suppression or antispasmodics. Other causes of abdominal pain must be excluded. Standard work-up includes endoscopic retrograde cholangiopancreatography (ERCP) with biliary manometry, which risks post-ERCP pancreatitis, especially in young women with normal bile ducts and liver serology. Noninvasive tests for SOD, such as timed ("gated") cholecystokinin (CCK)-stimulated hepatobiliary iminodiacetic acid (HIDA) scans and secretin-stimulated magnetic resonance cholangiopancreatography, are imperfect and still evolving. Although many doubt the very existence of SOD, a multidisciplinary approach to the management of pre- and postcholecystectomy abdominal pain syndromes is long overdue.

Reduced gallbladder ejection fraction (GBEF) with normal laboratory tests and no gallstones on ultrasound can be attributed to conditions such as biliary dyskinesia, chronic acalculous cholecystitis, cystic duct syndrome, sphincter of Oddi dysfunction, and subclinical biliary stricture. We present a case of a patient with chronic right upper quadrant pain, diagnosed with reduced GBEF, normal labs, and no gallstones. The patient's symptoms resolved after endoscopic retrograde cholangiopancreatography and sphincterotomy, revealing a mild, non-obstructive stricture in the middle third of the common bile duct. This case underscores the importance of considering ERCP and sphincterotomy as diagnostic and therapeutic options before opting for cholecystectomy in patients with reduced GBEF and normal lab results, potentially avoiding unnecessary surgical interventions.

What is the role of the cholecystokinin stimulated HIDA scan in evaluating abdominal pain in children?

To characterize functional biliary pain and other gastrointestinal (GI) symptoms in postcholecystectomy syndrome (PCS) patients with and without sphincter of Oddi dysfunction (SOD) proved by endoscopic sphincter of Oddi manometry (ESOM), and to assess the post-endoscopic sphincterotomy (EST) outcome. We prospectively investigated 85 cholecystectomized patients referred for ERCP because of PCS and suspected SOD. On admission, all patients completed our questionnaire. Physical examination, laboratory tests, abdominal ultrasound, quantitative hepatobiliary scintigraphy (QHBS), and ERCP were performed in all patients. Based on clinical and ERCP findings 15 patients had unexpected bile duct stone disease and 15 patients had SOD biliary type I. ESOM demonstrated an elevated basal pressure in 25 patients with SOD biliary-type III. In the remaining 30 cholecystectomized patients without SOD, the liver function tests, ERCP, QHBS and ESOM were all normal. As a control group, 30 'asymptomatic' cholecystectomized volunteers (attended to our hospital for general cardiovascular screening) completed our questionnaire, which is consisted of 50 separate questions on GI symptoms and abdominal pain characteristics. Severity of the abdominal pain (frequency and intensity) was assessed with a visual analogue scale (VAS). In 40 of 80 patients having definite SOD (i.e. patients with SOD biliary type I and those with elevated SO basal pressure on ESOM), an EST was performed just after ERCP. In these patients repeated questionnaires were filled at each follow-up visit (at 3 and 6 mo) and a second look QHBS was performed 3 mo after the EST to assess the functional response to EST. The analysis of characteristics of the abdominal pain demonstrated that patients with common bile duct stone and definite SOD had a significantly higher score of symptomatic agreement with previously determined biliary-like pain features than patient groups of PCS without SOD and controls. In contrary, no significant differences were found when the pain severity scores were compared in different groups of PCS patients. In patients with definite SOD, EST induced a significant acceleration of the transpapillary bile flow; and based on the comparison of VASs obtained from the pre- and post-EST questionnaires, the severity scores of abdominal pain were significantly improved, however, only 15 of 35 (43%) patients became completely pain free. Post-EST severity of abdominal pain by VASs was significantly higher in patients with predominant dyspepsia at initial presentation as compared to those without dyspeptic symptoms. Persistent GI symptoms and general patient dissatisfaction is a rather common finding after EST in patients with SOD, and correlated with the presence of predominant dyspeptic symptoms at the initial presentation, but does not depend on the technical and functional success of EST.

Gallbladder Function Before and After Fundoplication