Abstract

Pancreatitis is not one disease but several and perhaps many. Diagnosis is imperfect in all forms and the usual lack of histologic material has hampered attempts to understand the pathogenesis and possible interrelationships of the different forms of pancreatic inflammation. Acute pancreatitis does not as a rule evolve into chronic pancreatitis, even after multiple recurrences. Recurrent acute attacks can be ended by identifying and treating the factor causing the disease, including recently recognized entities such as accessory papilla stenosis associated with pancreas divisum. Attempts to improve the treatment of severe acute pancreatitis are focussing upon preventing injury to pancreatic cell structures, enhancing endogenous mechanisms for capture and disposal of activated enzymes, and upon early detection and debridement of damaged pancreatic and peripancreatic tissues. Pancreatic duct stricture or obstruction as a consequence of scarring from necrotizing pancreatitis may produce recurrent symptoms, now designated as obstructive pancreatitis. Obstructive pancreatitis has its own unique histologic characteristics and is appropriately treated by resection of the blocked segment of pancreas when the point of obstruction is distal to the papilla. Chronic pancreatitis differs from acute or obstructive pancreatitis in that it is difficult or impossible to halt its progression. The role of intraductal protein precipitates, whether of enzymes or perhaps of other unique pancreatic secretory proteins, in the pathogenesis of the disease is being evaluated. The goal of surgical treatment is not to cure, but to reduce pain, overcome associated obstruction of the bile duct or duodenum, and to treat pancreatic duct disruptions including pseudocysts and internal pancreatic fistulas. Because continuing deterioration of pancreatic function is to be expected in chronic pancreatitis, maximum conservation of pancreatic tissue by avoiding resectional procedures is advisable.

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