ACUTE HEMORRHAGIC PANCREATIC NECROSIS PRODUCED BY LOCAL SHWARTZMAN REACTION

Abstract

Histological observations in cases of fatal hemorrhagic pancreatic necrosis consistently show extensive vascular injury. These lesions vary from diffuse hyaline capillary thrombosis to extensive necrosis of arterioles, venules, and larger vessels.¹Frequently there is accompanying hemorrhage, thrombosis, and inflammatory cell infiltration. Whether the vascular lesion is the result of exposure to liberated trypsin or is, indeed, the primary factor producing hemorrhagic pancreatitis is not yet clear.^1b In studying the dermal Shwartzman reaction it became apparent that there was a striking similarity between this rapidly developing vascular lesion and that of acute hemorrhagic pancreatitis. Accordingly, the present study was undertaken with the object of evaluating the role of primary vascular sensitization in the pathogenesis of hemorrhagic pancreatitis. The experiments herein reported demonstrate the permeability of the pancreatic ductal system to bacterial products perfused within the physiological pressure range and the ability of such products to sensitize the pancreatic blood