Pancreatic inflammation comprises a variety of pathological forms, each of which has received extensive clinical and experimental study. One of the principal problems, still unsolved, involves the mechanism responsible for the initiation of pancreatic necrosis. Necrotizing pancreatitis usually begins with clinical findings similar to those encountered in less serious types of pancreatic inflammatory disease. Acute abdominal pain often follows excessive consumption of food or drink, and the correct diagnosis may be confused with other acute abdominal situations, such as cholecystitis or ruptured viscus. The condition of the patient deteriorates rapidly to a stage of shock, overwhelming toxicity, and, frequently, death, despite aggressive treatment. Pathological findings in acute pancreatic necrosis are most impressive. The abdomen and retroperitoneal tissues are filled with serosanguinous fluid, and foci of fat necrosis are usually distributed diffusely. The pancreas is swollen, boggy, necrotic, and distended with bloody fluid. Microscopic changes include severe edema, leukocytic infiltration, patchy