DISTURBANCES OF PANCREATIC METABOLISM G87 



Opie reported a case of acute pancreatitis at which at autopsy a small 

 gall stone was found impacted in the common bile duct near the papilla. 

 The lesser peritoneal cavity was the site of an abscess surrounded by fat 

 necrotic tissue. The face of the pancreas was covered bv hemorrhage. 

 Opie collected many similar cases from the literature in which gangrenous 

 or hemorrhagic pancreatitis was associated with gall stones lodged at or 

 near the common orifice of the ducts. 



A second case furnished Opie(c) with the mechanism by which a pan- 

 creatitis was produced. In this case, the diverticuhim of Vater was un- 

 usual in length, 10 mm. ; the orifice into the duodenum measured 5 mm. 

 In the diverticulum was found a calculus 3 mm. in diameter. Such a 

 calculus by plugging the Vaterian orifice would convert the common bile 

 duct and pancreatic ducts into a continuous open channel and thus divert 

 the bile into the Wirsungian or associated ducts. This is the mechanism 

 advanced by Opie as explaining the phenomenon. 



Not alone the impaction of a gall stone in the common duct is essential 

 for in many cases, apart from trauma, no gall stones are found. In 

 recent years study has been directed toward the sphincter of Oddi, the 

 sphincter that guards the papilla of Vater at its point of junction with 

 the duodenum. Meltzer attributed to spasm of this sphincter some forms 

 of obstructive jaundice and its importance in regulating the expulsion 

 of bile and pancreatic juice has come more and more into the foreground. 

 The experiments of Williams and Busch show that by passing glass balls 

 through the sphincter, dilatation of the sphincter was caused with re- 

 sultant pancreatic necrosis, due to regurgitation of intestinal contents. 

 It had been previously shown that duodenal stasis alone would not cause 

 regurgitation into the ducts when the sphincter was intact (Seidel). 

 The added injury to the sphincter caused by the glass balls, analogous to 

 gall stones, might well be one of the deciding factors. 



Archibald showed that experimentally a pressure of even 1000 mrn. 

 of water in the gall bladder was unable to force an iron solution iiLto the 

 pancreatic ducts, when the sphincter was ligated. However, a pressure 

 within the bile ducts of from 300 to 800 mm. of water was sufficient to 

 flood the pancreatic ducts. If the bile salts alone or sterile bile was used a 

 moderate reaction comparable to a subacute pancreatitis resulted; if to 

 the bile there was added a bacterial culture, a severe acute pancreatitis 

 necrosis and death resulted, in one cat within twenty minutes. Archibald 

 attributed the necrosis of the pancreas to the chemical action of the irri- 

 tant employed. Infected bile acted not by bacterial activity but by the 

 chemical changes produced in the bile by the innoculated bacteria. 



Opie(&) experimentally reproduced pancreatic necrosis in animals by 

 injecting sterile bile into the pancreatic ducts, subsequently ligaturing 

 the orifice of the duct. Hemorrhagic pancreatitis and fat necrosis resulted. 



