Abstract
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Introduction: Chronic acalculous cholecystitis (CAC) is due to inflammation of the gallbladder wall which can lead to impaired GB contraction/emptying. Hepatobiliary scintigraphy with intravenous cholecystokinin (CCK) administration is commonly used to confirm the clinical diagnosis of CAC by demonstrating a reduced gallbladder ejection fraction (EF) response to CCK. The current recommendation for CCK administration calls for the infusion of sincalide at 0.02µg/kg over a 60-minute duration (1). This differs from the previous version of the protocol where the same amount of sincalide (0.02µg/kg) was infused over a 3-minute period. The change to the longer 60-minute sincalide infusion rate occurred as there were concerns that the 3 minute infusion protocol might result in increased false positive rates which may lead to unnecessary surgery. It was also changed as the longer infusion rate is currently believed to be the optimal method to quantify gallbladder contraction and emptying (2,3). To the best of our knowledge, no study has yet evaluated the efficacy of the 60-minute sincalide protocol in detecting symptomatic CAC. The purpose of this study is to determine it.
Methods: We retrospectively reviewed the findings of 966 patients who underwent a CCK hepatobiliary scan between 2012 and 2016 to determine their 60-minute ejection fraction response to CCK. These studies were performed in the nuclear medicine divisions of the Beaumont Health hospital system. From this cohort of patients, only those who had a CCK hepatobiliary scan and cholecystectomy within 6 months (183 days) of each other were included in our analysis (n=71). Each patient underwent a 60-minute infusion protocol to determine their 60-minute gallbladder EF response to CCK. Patients were categorized as either having a normal (EF greater than or equal to 38%) or abnormal (EF less than 38%) gallbladder EF response to CCK. The patients’ post-cholecystectomy histopathology results were then reviewed for the presence of gallbladder disease. Only patients who were reported to have or not have CAC were included in our final analysis (n=28). Those with other gallbladder pathology were excluded (e.g. cholelithiasis, cholesterolosis, acute cholecystitis, polyps, or adenomyoma). From this data the sensitivity, specificity, positive predictive value, and negative predictive value of CCK cholescintigraphy in detecting symptomatic CAC was determined.
Results: Of the 966 total patients who underwent CCK hepatobiliary scintigraphy, 71 had a cholecystectomy within 6 months of their CCK hepatobiliary scan and had pathology results available for review in the electronic medical record system. Of those 71 patients, 28 were reported to have or not have histopathology findings of CAC without additional gallbladder pathology. These patients were categorized into one of four different groups; abnormal EF on hepatobiliary scintigraphy with CAC on histopathology (true positive), abnormal EF without CAC (false positive), normal EF with CAC (false negative), or normal EF without CAC (true negative). Of the 28 evaluated patients; there were 17 true positives, 2 false positives, 7 false negatives, and 2 true negatives resulting in a sensitivity of 71%, specificity of 50%, positive predictive value of 89%, and negative predictive value of 22% (Table 2). Age, sex, gallbladder EF, and time to surgery (days) are shown in Table 1.
Conclusions: Our findings suggest that a 60-minute sincalide infusion protocol results in/maintains a high positive predictive value for identifying symptomatic CAC; a finding similar to our previous 3-minute sincalide infusion protocol (3). Its poor sensitivity, specificity, and negative predictive value limits its utilization to only confirming histopathologic CAC in patients clinically suspected of having it. Further studies need to be performed to confirm this as only 28 patients were evaluated as well as ensuring, another limitation of this study, post-cholecystectomy symptom resolution.
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