THE PATHOLOGIC anatomy of animals and human beings with acute pancreatitis (pancreatic necrosis) often manifests widespread thromboses, infarctions and hemorrhages, and there is reason to believe that disruption of the blood supply to the parenchyma of the pancreas is necessary for the progression of the lesion from pancreatic edema to pancreatic necrosis.1 Rich and Duff2 have shown changes in the medial coat of small arteries within the organ and elsewhere in the body in instances of pancreatitis in man and experimental animals, and they expressed the belief that this damage is specifically due to activated trypsin, a substance which has long been suspected of playing a major role in the dramatic pathologic changes seen in cases of this malady. However, in some classic examples of pancreatic necrosis this vascular lesion has not been demonstrable, which suggests that other factors may be operative in inducing thrombosis and hemorrhage. One
LASHER EP, McCABE MM. CHANGES IN COAGULATION TIME ASSOCIATED WITH EXPERIMENTAL ACUTE PANCREATITIS IN DOGS. Arch Surg. 1950;60(1):164–169. doi:10.1001/archsurg.1950.01250010180017
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