690 BURRILL B. CROHN 



blood was increased. They assumed "that death was due to flooding of 

 the blood stream with higher split products formed at the expense of the 

 pancreatic tissue, of which the proteose increase is an index." They 

 found a definite increase in the antiferment content of the blood and re- 

 garded this as a protective phenomenon favoring recovery. The injection 

 of trypsin into the duct gave the picture of a true tryptic shock with fatal 

 result ; serum protein was markedly increased, while the protective tryptic 

 antiferment had markedly diminished. Injection of soaps into the duct 

 gave a less severe and quite different reaction. 



Goodpasture(6), by chemical means, separated from the fresh normal 

 pancreas of a dog a thermostabile toxic element, present in the (3-nucleo- 

 protein fraction, probably protein in nature. Minute doses of the puri- 

 fied substance produced in dogs symptoms comparable to spontaneous 

 hemorrhagic necrosis of the pancreas. 



Is the peritoneal exudate that occurs in toxic pancreatic necrosis itself 

 toxic and what are the virtues of operative interference for draining this 

 exudate ? To this hypothesis Whipple and Goodpasture devoted them- 

 selves. They demonstrated the presence of protective antiferments in 

 the serum and blood plasma in experimental pancreatitis. 



The peritoneal exudate of a dog suffering from experimental pan- 

 creatic necrosis was injected intraperitoneally into a healthy animal. 

 The dog remained well. Nor was a toxic effect seen when the peritoneal 

 exudate was injected intravenously. 



In a dog suffering from the effects of a severe hemorrhagic pancreatitis 

 the peritoneal exudate of a similarly affected dog was injected intra- 

 venously and again intraperitoneally without increasing the gravity of 

 the symptoms. In fact the dogs from whom the exudate was taken re- 

 mained more sick than those into whom it was injected, the latter recover- 

 ing completely. 



They conclude that the peritoneal exudate is one of the protective phe- 

 nomena of pancreatic necrosis, and that its operative removal and drainage 

 is not only dangerous but needless. 



From the mass of the above detail experimental and clinical data one 

 may deduce the modus operandi of hemorrhagic pancreatitis and necrosis 

 in the following manner. Intrapancreatic activation of protrypsin and 

 steapsin takes place due to the entrance of infected bile or intestinal secre- 

 tion or perhaps spontaneously ; or again in traumatic cases by bruising 

 or rupture of the intestine. The activated ferments cause necrosis and 

 autolysis of the parenchyma with the absorption of . an unknown toxic 

 agent, in all likelihood proteose in nature. The degree of damage to the 

 secreting cells determines the degree of necrosis, gangrene, or hemorrhagic 

 destruction (damage to the blood vessels) that will ensue. The body 

 reacts to the absorption of the toxic protein by increase of anti-ferment in 

 the blood, by the appearance of protective specific substances in the blood 



