Diagnosing infected necrotizing pancreatitis: Clinical signs, gas bubbles or routine fine-needle aspiration?

Abstract

Introduction: Infection of pancreatic necrosis in necrotizing pancreatitis increases the lethality. Aims/objectives: To examine the mechanisms underlying this clinical circumstance we used a model of primary infected pancreatic necrosis in taurocholate induced pancreatitis in mice. Materials and methods: Acute necrotizing pancreatitis with sterile necrosis (SN) was induced by retrograde injection of 4% taurocholate in the common bile duct of Balb/c mice, infected pancreatic necrosis (IN) was induced by co-injecting 108 CFU E. coli. For antibiotic therapy 10 mg/kg bodyweight moxifloxacin were administered intravenously (AIN). After 6, 12, 24, 48 and 120 hours animals were sacrificed and serum as well as SIRS related organs were examined. Results: Prolonged bacteremia occurred when infected acinar cell necrosis was induced (24h CFU E. coli in blood; bacteria only not detected, IN 121 63). Infection of pancreatic necrosis with E. coli further increased the pancreatic damage (histology score 24h: SN 17.8 2.6 vs. IN 23.7 2.2; p<0.001) and the systemic complications such as the pulmonary vascular leak (albumin in bronchoalveolary lavage 6h: SN 151.0 57.7 mg/ml vs. IN 219.5 76.2 mg/ml; p<0.05). Additionally, infected necrosis induced impaired hepatic function with reduced serum glucose concentrations (24h: SN 167.0 35.6 mg/dl vs. IN 106.9 12.7 mg/dl; p<0.001). Moxifloxacin treatment reduced the systemic inflammatory response (serum IL-6: IN 330.5 336.6 vs. AIN 38.7 25.5 pg/ml; p<0.001) and restored liver function (serum glucose: IN 105.8 12.7 vs. AIN 155.7 39.5 mg/dl; p<0.001). Conclusion: Infection of pancreatic necrosis induces sustained bacteremia and increases the systemic complications in acute necrotizing pancreatitis. Initial antibiotic therapy reduces the inflammatory response and restores liver function.