Surgical Pancreas Liver and Shunt Procedures with CC

Pancreatitis, acute or chronic, is an inflammation and potential necrosis of the pancreas. Tissue damage from pancreatitis occurs because of activation of proteolytic and lipolytic pancreatic enzymes that are normally activated in the duodenum. Proteolytic enzymes, such as trypsin, elastase, and phospholipase, break down protein; lipolytic enzymes break down fats. The enzymes cause autodigestion (destruction of the acinar cells and islet cell tissue), with leakage of the enzymes and fluid into surrounding tissues. The pancreas can return to normal after an attack of acute pancreatitis with successful treatment, or it may progress to a state of chronic inflammation and disease.

The mortality rate of people with acute pancreatitis is as high as 15%, but in patients with severe disease, it can reach 30%, particularly when people develop multiple organ dysfunction syndrome (MODS). In chronic pancreatitis, there is permanent destruction. Precipitation of proteins causes pancreatic duct obstruction. Edema and distension cause damage and loss of the acinar cells, which normally produce digestive enzymes. The normal cells are replaced with fibrosis and necrosis. As the autodigestion process of the pancreas progresses, the cells form walls around the fluid that contains enzymes and the necrotic debris. These pseudocysts can rupture into the peritoneum and surrounding tissues, resulting in complications of infection, abscesses, and fistulae. The islet cells within the pancreas may also be damaged and destroyed, leading to diabetes mellitus. Other complications include massive pancreatic hemorrhage and shock, acute respiratory distress syndrome, atelectasis, pleural effusion, pneumonia, paralytic ileus, and rarely, cancer.

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