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Pathophysiology, diagnosis, and assessment of acute pancreatitis 

Pathophysiology, diagnosis, and assessment of acute pancreatitis
Pathophysiology, diagnosis, and assessment of acute pancreatitis

James R. A. Skipworth

and Stephen P. Pereira

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date: 21 May 2022

The incidence of acute pancreatitis continues to increase, but the attendant mortality has not decreased for >30 years. The pathogenesis remains poorly understood, but the initial mechanism appears to be intracellular activation of pancreatic enzymes, with micro- and macrovascular dysfunction, in conjunction with a systemic inflammatory response acting as a key propagating factor and determinant of severity. A multitude of causes or initiators exist, but there is a common pathophysiological pathway. The use of conventional scoring systems, combined with repeated clinical and laboratory assessment, remain the optimal method of predicting early severity and organ dysfunction. Death occurs in a biphasic pattern with early mortality (<2 weeks) secondary to SIRS and MODS; and late deaths (>2 weeks) due to superinfection of pancreatic necrosis. Assessment of severity should reflect this, with early severity being diagnosed in the presence of organ failure for >48 hours, and late severity defined by the presence of pancreatic and peri-pancreatic complications on CT or other appropriate imaging modalities.

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