The exact genesis of acute hemorrhagic pancreatitis is unknown, although it has been the subject of repeated clinical and experimental study. In 1855 Claude Bernard1 first attempted to produce hemorrhagic pancreatitis in dogs by injecting bile mixed with sweet oil into the pancreatic duct. Ever since this early study many methods for producing the disease have been employed, none of which completely demonstrate the pathogenesis.
Rich and Duff2 concluded that obstruction and subsequent distention and rupture of pancreatic ductules with a resultant escape of pancreatic juice into the interstitial tissue is the cause of edematous pancreatitis. They further stated that necrosis of the walls of neighboring arteries and veins transforms edematous pancreatitis into hemorrhagic pancreatitis. Archibald,3 Cameron,4 and Opie5 consider that obstruction at the papilla of Vater by stone or spasm with reflux of bile through a common channel into the pancreatic duct is the
KELLY TR, BRATCHER EP, FALOR WH, CATRON L, REYES LB. Experimental Pancreatitis: Synchronous Production in Normal and in Ectopic Pancreas. Arch Surg. 1963;87(6):988–992. doi:https://doi.org/10.1001/archsurg.1963.01310180104018
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