[Etiology and pathophysiology of acute pancreatitis]

The pathophysiology of acute pancreatitis can be divided into four different pathogenetic principles. 1. Ductular: The ductular pathogenesis is characterized by the frequent association between migrating gallstones and acute pancreatitis. The causative mechanism consists of an intraductal pressure and permeability increase with consecutive premature enzyme activation. 2. Acinar: The acinar pathogenesis is based on autoactivation of pancreatic enzymes after misdirected basolateral secretion into the interstitium of the pancreas and/or by colocalization of lysosomes and proenzyme-rich zymogen granules inside the acinar cell. 3. Mixed ductular-acinar: The main entity of this pathophysiological concept is the acute alcohol pancreatitis. An increase of intraductal pressure, of duct permeability and a possible direct toxic effect seem to be responsible. 4. Microcirculation disturbance: An impairment of pancreatic microcirculation appears to play a key role in the progression of edematous to necrotizing pancreatitis and was demonstrated in all models of necrotizing pancreatitis examined so far. Causative factors are poor blood fluidity by hemoconcentration, intravascular hypercoagulability, an impairment of arteriolar inflow by vasospasms, of capillary flow by direct endothelial injury and edema, of venous outflow by thrombosis, leukocyteendothelium interaction and direct toxic injury by activated enzymes, kinins and other mediators. A specific and therapeutically successful approach represents the administration of dextran which antagonizes both systemic and local causes of microcirculatory impairment.