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Abstract

The majority of patients with acute pancreatitis, particularly those with acute biliary pancreatitis suffer a mild disease; however 15–25 % develop severe acute pancreatitis, most of them in conjunction with a necrotizing course (Beger and Rau 2007). Abnormal intra-acinar calcium activity and premature activation of zymogens lead to autodigestion of the gland and local inflammation. Mild acute pancreatitis is dominated by intra-pancreatic oedema, spreading cell necrosis, accumulation of inflammatory cells, and local release of pro-inflammatory cytokines (Mayer et al. 2000; Poch et al. 1999). Using multi-slice contrast enhanced CT (CECT), necrotizing pancreatitis is defined by the presence of focal or extended necrosis; but even mild, acute oedematous-interstitial pancreatitis may be associated with some cell necrosis throughout the pancreas, despite the CECT showing only enlargement of the pancreas (Balthazar et al. 1990). Based on wet weight of the removed necrosis in patients undergoing debridement, extended necrosis (>180 g wet weight) is present in about 30 % of patients ultimately requiring operative intervention for necrotising pancreatitis. Infection of the necrosis occurs in about 20–35 % of all patients with necrotizing pancreatitis (Table 21.1). The necrotizing tissue process occurs in the first few days of the disease and does not appear to occur later on in the disease process.

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Correspondence to Hans G. Beger .

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Beger, H.G., Rau, B.M., Poch, B. (2013). Commentary. In: Mantke, R., Lippert, H., Büchler, M., Sarr, M. (eds) International Practices in Pancreatic Surgery. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-540-74506-8_21

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  • DOI: https://doi.org/10.1007/978-3-540-74506-8_21

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