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by Kathryn Lindsey, M.D.
Acute pancreatitis is typically defined as reversible inflammatory injury to the pancreas and refers to a spectrum of disease. In the United States, the most common causes of acute pancreatitis are alcohol abuse and biliary tract disease, with physical, chemical, infectious, or ischemic injuries being more rare causes. Presentation of disease ranges from elevated pancreatic enzymes without physical symptoms to severe epigastric pain. Such variability has lead to the development of the Ranson Criteria which lends prognostic significance to laboratory findings.
The overall mortality rate of acute pancreatitis is low; however, it remains a well-recognized cause of sudden, unexpected death. The following images show the microscopic pathological findings from such a case. This decedent had complained for several weeks of abDominal pain and vomiting before being found dead at his residence. He had a history significant for both chronic ethanol use and gall stones.
Figures 1 and 2 illustrate the common aberrations seen in acute pancreatitis. From low power one can see hemorrhage, necrosis, and fat necrosis while at high power one can see that acute inflammatory cells have infiltrated the pancreatic parenchyma, attacking acini, ducts, and islets and leaving necrotic debris in their wake. Proteolytic digestion of the tissue damages the blood vessels resulting in interstitial hemorrhage and edema. Lipolytic enzymes digest the peripancreatic fat causing fat necrosis, and in more severe disease, the resultant free fatty acids will combine with ionic calcium and precipitate. It is pertinent to note that the pathogenesis of acute pancreatitis is thought to be an autodigestive process. As autopsy specimens frequently suffer autolysis, one should look for hemorrhage and acute inflammation to distinguish acute pancreatitis from simple autolysis.