FAT NECIiOSIS 387 



ereatic trypsinojren sufficiently to make it highly toxic These ob- 

 servations indicate that in pancreatic necrosis it is the kinase liberated 

 from the autoly/.in<r necrotic tissue -wliich is responsil)]e for the acti- 

 vation and resultin": toxic effects of the trypsinopren. As a result of 

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

 (lead 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 canned 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 

 necrosis.- Fat necrosis itself is not dangerous to the affected organ- 

 ism, the associated pancreatitis fand peritonitis) causing all the 

 symptouis.^ There is no evidence that sufficient quantities of soaps 

 (which are toxic) are absorbed from the necrotic areas to cause appre- 

 ciable intoxication. The soaps that are formed in the necrotic areas, 

 indeed, are probably not much absorbed, but are precipitated as cal- 

 cium soaps ; in such areas at least as high as 85 per cent, of the soaps 

 may be insoluble.* Healing follows rapidly in case of recovery ; the 

 foci may disappear as early as eleven days after their formation (in 

 experimental animals). 



In the urine of persons with pancreatitis is frequently found a 

 substance forming an osazone, which has been the subject of much 

 investigation because of its possible diagnostic value. Cammidge,^ 



iPavr and Martina. Dent. Zeit. Chir., 1006 (F.3), 189. 



2 See Berner. Virchow's Arch., 1007 (187), .300. 



3 Giileke (Arch. klin. Chir., 1008 (8,5), 015) considers the intoxication of acute 

 pancreatitis as an intoxication Avith trvpsin. A\liich can be checlced bv antitrAjisin. 

 Doberauer (Beitr. klin. Chir.. lOOG (48), 450), Esdahl (.Tour. Exp. Med.'. 1007 

 (0). .385), and Petersen, .Tol)lin£r, and Egprstein. ibid., 1016 (23), 401, however, 

 look upon tlie products of cellular disintegration as the source of tlie intoxica- 

 tion. V. Bercruiann (Zeit. exp. Path. u. Ther.. 1006 (3), 401, states that the 

 toxicity is not due to either tlie enzymes or to allnimoses; and that it is a true 

 autointoxication Avhich can be prevented by ^irevious immunization witli either 

 pancreas extracts or commercial trvpsin. (See also Fischler, Deut. Arch. klin. 

 Med., 1011 (103). 156: and v. Bergmann and Culeke, IMiinch. med. Woch., 1010 

 (57), 1673). The histones and protamines liberated from the digested tissue, 

 and which are very toxic, have been sugprested as a possible factor by Schitten- 

 helm and Weichardt (Zeit. Immunitiit.. 1013 (14), 600), while the beta-nucleo- 

 proteins are inchided among the toxic elements bv Goodpasture. Jour. Exp. Med.. 

 1017 (25), 277. 



4 See Frugoni and Stradiotti, Arch. Sci. !Med., Torino, lOlO; also Berl. klin. 

 Woch.. 1010 (47). 386. 



sProc. Royal Soc. Med., 1010 (III, pt. 2), 103, bibliographv: Lancet, 1014, 

 Sept. 26. ... 



