Specific aspects of acute pancreatitis

Acute pancreatitis (AP) is still a disease with a significant mortality rate, mainly concerning the severe forms of this disease. Mortality in acute pancreatitis has 2 peaks. The first peak is caused by systemic inflammatory response syndrome (SIRS), which takes place in the first week of the disease. Sepsis is responsible for a second peak. It begins 1 to 3 weeks after the onset of acute pancreatitis and is caused by pancreatic superinfection. Sepsis as a result of infected pancreatic necrosis is the most serious complication in late phase of severe acute pancreatitis (SAP) and contributes to the high mortality rate of this disease. This complication is thought to be a result of the bacterial translocation from the gastrointestinal tract. The damage of the microvessels and the subsequent onset of systemic cascade reactions plays also an important role during acute pancreatitis. Recent experimental data suggest also the role of nervous system in etiopathogenesis of acute pancreatitis. We assume that the diagnostic and treatment strategy can not improve without a thorough knowledge of the physiology and patophysiology of acute pancreatitis. Therefore the aim of this paper is to highlight certain specific situations of high importance that are activated in the human organism during acute pancreatitis (Ref. 100).