PATHOLOGY OF ACUTE PANCREATITIS

PATHOLOGY
Detailed histological studies of pancreatic tissue are available from a limited number of cases of human acute pancreatitis. A histological spectrum of acute pancreatitis is recognized ranging from mild, interstitial disease to coagulation necrosis. 3 Interstitial pancreatitis may lead to local and systemic complications but is rarely fatal; necrotizing pancreatitis may be fatal in up to 30% of cases.

Interstitial
In interstitial pancreatitis the gland is edematous, but its gross architecture is preserved. Parenchymal inflammatory cells are present together with interstitial edema. Disruption of the normal acinar cell architecture is common and may contribute to the reduced enzyme secretion characteristic of acute pancreatitis. Zymogen granules are displaced from their fusion site in the apical domain of the cell and become dispersed throughout the cell, and the apical membrane appears contracted and microvilli disappear. 4 Zymogen granules fuse with each other instead of the apical membrane. Similar to animal models of pancreatitis, a distinct form of cell necrosis is observed in which the apical domain of the acinar cell is shed into the lumen, resulting in intact zymogen granules within the lumen. This pattern of partial cell necrosis may allow the acinus to regenerate rapidly after injury.

Necrotizing
Macroscopically, marked tissue necrosis and hemorrhage are apparent. Surrounding areas of fat necrosis are also prominent. These chalky areas of dead adipose tissue are found within the peripancreatic tissue and throughout the abdomen. Large hematomas often are located in the retroperitoneal space. The microscopic appearance of the pancreas parallels the gross changes, with marked fat and pancreatic necrosis. Vascular inflammation and thrombosis are common.