PANCREATIC FAT NECROSIS 389 



about four hours a substance appears in the decomposed fat that 

 stains with hematoxylin, which is probably calcium. 



Fat necrosis may be produced by any means that will cause the 

 escape of pancreatic juice from the natural channels within the 

 gland. In human pathology it has followed trauma and acute in- 

 fection of the gland, and the blocking of the ampulla of Vater by gall- 

 stones which permits the bile to back up into the pancreatic duct, 

 where it produces an acute inflammation of the pancreas (Opie).^^ 

 Flexner^^ has shown that it is the bile salts that cause the inflamma- 

 tion, and also that this effect is decreased or prevented by the presence 

 of large amounts of colloids. Much emphasis is laid by some au- 

 thors^^ upon the necessity of enterokinase passing up the ducts to 

 activate the trypsinogen (an idea first advanced by Starling and Bay- 

 liss in 1902), but it should be remembered that there are kinases pres- 

 ent in leucocytes, and that kinases can develop in the pancreas itself 

 during autolysis, which can activate the trypsinogen; hence the pres- 

 ence of e nter o-kinase is not essential for sufficient activation of tryp- 

 sinogen to account for pancreatitis and fat necrosis. Lattes^* believes 

 that fresh pancreatic juice, which digests tissues very slowly, can pro- 

 duce typical fat necrosis but not the characteristic intoxication; this 

 results from the action of juice which has been activated by entero- 

 kinase, or by products of pancreatic autolysis which have a similar 

 effect. The kinases of leucocytes he found unable to activate pan- 

 creatic trypsinogen sufficiently to make it highly toxic. These ob- 

 servations indicate that in pancreatic necrosis it is the kinase liberated 

 from the autolyzing necrotic tissue which is responsible for the acti- 

 vation and resulting toxic effects of the trypsinogen. As a result of 

 injury by bile salts, or any other agent that produces cell death, the 

 dead and injured cells are digested by the pancreatic juice which is 

 thus further activated and makes its escape into the surrounding fat 

 tissue. Wells' experiments showed that the lesions of fat necrosis 

 may be produced in three to five hours, large enough to be visible to 

 the naked eye; their form and size depend solely upon the area of fat 

 tissue exposed to the action of the pancreatic juice. The process 

 progresses for but a few hours, the extension seeming to be limited by 

 surrounding leucocytes. The lesions may appear at remote points in 

 the thoracic and pericardial cavities or in the subcutaneous tissues, 

 the causative agent probably being carried by the lymphatic vessels, 

 possibly in the form of emboli of pancreas cells. ^^ There may even be 

 some splitting of the fats in the liver in these cases, with intrahepatic 



" Bull. Johns Hopkins Hosp., 1901 (12), 182. 

 32 Jour. Exp. Med., 1906 (S), 167. 



33P61ya, Mitt. Grenz. Med. u. Chir., 1911 (24), 1; Rosenbach, Arch. klin. 

 Chir., 1910 (93), 278. 



^* Virchow's Arch., 1913 (211), 1. 



35Pavr and Martina, Deut. Zeit. Chir., 1906(83), 189. 



