Acute Pancreatitis after Embolization of Liver Tumors: Frequency and Associated Risk Factors

Introduction: Acute pancreatitis (AP) is a rare complication after liver embolization (LE) of primary and secondary liver tumors (approximately 1.7%), but it has a significant morbidity and mortality potential if associated with other complications. It usually develops early within 24 h after the LE procedure. Study Purpose: To calculate the frequency of AP after LE in our institution and to analyze the factors involved in this procedure (anatomical features, embolization materials, cytostatic drugs, technical factors). Materials and Methods: 118 LE (bland embolization and transarterial chemoembolization) were performed in our institution. The study group included 59 patients who met the following inclusion criteria: one or more LE events, with complete pre- and post-in-terventional laboratory studies including: serum Ca2+>, creatinine, blood urea nitrogen, glucose, lactatedehydrogenase, aminotransferases, alkaline phosphatase, amylase, lipase, C-reactive protein, hematocrit and leukocytes. The diagnosis of AP was established according to the criteria of the Atlanta system of classification. For the statistical analysis the association between two response variables (e.g. AP after embolization and risk factor during the embolization, AP after embolization and volume of embolic material) was evaluated using Pearson's χ2 test and Fisher's exact test. Results: The calculated frequency of AP after LE in our series was 15.2%. Amylase and lipase were elevated up to 8.7 and 20.1 times, respectively, 24 h after LE. We observed a statistically significantly lower incidence of AP in those patients who received 2 ml or less of embospheres compared with those with an embolization volume of >2 ml (Pearson's χ2 = 4.5000, Pr = 0.034, Fisher's exact test = 0.040). Although carboplatin was administered to 7 of 9 of the patients who developed AP after the embolization procedure, there was no statistical significance (Fisher's exact test = 0.197) for carbo-platin as an AP risk factor when compared with all the patients who received this drug (n = 107). Conclusion: Although AP after LE seems to have a multifactorial etiology, both the toxicity of the antineoplastic drugs (carboplatinrelated toxicity) as well as direct ischemic mechanisms (non-target embolization, reflux mechanisms) may be the most important causes of the inflammatory pancreatic reaction after LE. We suggest that systematic measurement of serum pancreatic enzymes should be performed in cases of abdominal pain following selective LE and transarterial chemoembolization in order to confirm acute pancreatitis after embolization, which can clinically mimic a postembolization syndrome.