Optimal hepatobiliary scintigraphy for gallbladder dyskinesia.

BACKGROUND: The accuracy of hepatobiliary scintigraphy to assess gallbladder function remains controversial. National supply shortages of pharmaceutical-grade cholecystokinin led to the use of an oral fatty meal to stimulate gallbladder contraction during hepatobiliary scintigraphy. The goal of this study was to compare the predictive indices of cholecystokinin and fatty meal ingestion for stimulation of gallbladder contraction. METHODS: Patients evaluated with hepatobiliary iminodiacetic acid scan from 2014 to 2017 were reviewed and grouped based on testing stimulant (fatty meal versus cholecystokinin). Patients who later underwent cholecystectomy were selected for analysis. Hepatobiliary iminodiacetic acid results were correlated with surgical pathology and postoperative resolution of symptoms. Two-way statistical analysis was performed. RESULTS: A total of 359 patients underwent hepatobiliary iminodiacetic acid scan followed by cholecystectomy for biliary dyskinesia. Patients who received fatty meal stimulant (n = 86) were compared to those that received cholecystokinin (n = 273). Mean gallbladder ejection fraction during hepatobiliary iminodiacetic acid was 38% and 44% for the cholecystokinin and fatty meal groups, respectively, P = .073. Predictive metrics were not statistically different between groups with regard to pathology, symptomatic improvement, or accuracy. Symptomatic resolution (cholecystokinin-hepatobiliary iminodiacetic acid 78%, fatty meal-hepatobiliary iminodiacetic acid 68%; P = 0.058) and specificity (cholecystokinin-hepatobiliary iminodiacetic acid 26%, fatty meal-hepatobiliary iminodiacetic acid 44%, P = 0.417) were comparable in both testing groups. CONCLUSION: Stimulation of gallbladder contraction with a fatty meal during hepatobiliary iminodiacetic acid testing is a more affordable and reliable alternative to cholecystokinin for patients undergoing evaluation for gallbladder dysmotility.

Hepatic Steatosis After Neoadjuvant Chemotherapy for Pancreatic Cancer: Incidence and Implications for Outcomes After Pancreatoduodenectomy.

BACKGROUND: This study aimed to determine the incidence of new onset hepatic steatosis after neoadjuvant chemotherapy for pancreatic cancer and its impact on outcomes after pancreatoduodenectomy. METHODS: Retrospective review identified patients who received neoadjuvant chemotherapy for pancreatic adenocarcinoma and underwent pancreatoduodenectomy from 2013 to 2018. Preoperative computed tomography scans were evaluated for the development of hepatic steatosis after neoadjuvant chemotherapy. Hypoattenuation included liver attenuation greater than or equal to 10 Hounsfield units less than tissue density of spleen on noncontrast computed tomography and greater than or equal to 20 Hounsfield units less on contrast-enhanced computed tomography. RESULTS: One hundred forty-nine patients received neoadjuvant chemotherapy for a median of 5 cycles (interquartile range (IQR), 4-6). FOLFIRINOX was the regimen in 78% of patients. Hepatic steatosis developed in 36 (24%) patients. The median time from neoadjuvant chemotherapy completion to pancreatoduodenectomy was 40 days (IQR, 29-51). Preoperative biliary stenting was performed in 126 (86%) patients. Neoadjuvant radiotherapy was delivered to 23 (15%) patients. Female gender, obesity, and prolonged exposure to chemotherapy were identified as risk factors for chemotherapy-associated hepatic steatosis. Compared with control patients without neoadjuvant chemotherapy-associated hepatic steatosis, patients developing steatosis had similar rates of postoperative pancreatic fistula (8% (control) vs. 4%, p = 0.3), delayed gastric emptying (8% vs. 14%, p = 0.4), and major morbidity (11% vs. 15%, p = 0.6). Ninety-day mortality was similar between groups (8% vs. 2%, p = 0.08). CONCLUSION: Hepatic steatosis developed in 24% of patients who received neoadjuvant chemotherapy but was not associated with increased morbidity or mortality after pancreatoduodenectomy.