324 RETROGRESSIVE CHANGES 



duced 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 pro- 

 gresses 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 sub- 

 cutaneous tissues, the causative agent probably being carried by 

 the lymphatic vessels. Fat necrosis itself is not dangerous to 

 the affected organism, the associated pancreatitis (and peritonitis) 

 causing all the symptoms. 1 There is no evidence that suffi- 

 cient quantities of soaps (which are toxic) are absorbed from 

 the necrotic areas to cause appreciable intoxication. Apparently, 

 however, glycerine is absorbed in sufficient quantities to appear 

 in the urine, for on this basis Cam midge 2 has devised a method 

 of diagnosis of pancreatic lesions by examining the urine for 

 glycerin, the value of which Robson 3 has affirmed. Healing 

 follows rapidly in case of recovery ; the foci may disappear as 

 early as eleven days after their formation (in experimental 

 animals). 



Self-digestion of the pancreas occurs soon after death, and 

 the pancreatic juice may in this way bring about a postmortem 

 fat digestion that resembles somewhat the intravital fat necrosis 

 in its gross appearances, 4 and Wells found that the same changes 

 might be produced by injecting pancreatin into the bodies of 

 dead animals, or by keeping fat tissue in pancreatin solutions. 

 Wulff found that fatty acids were demonstrable by Benda's 

 method in the pancreas of nearly all cadavers. The process 

 differs from the intra vitam form in being less sharply circum- 

 scribed, and microscopically by the absence of cellular and vas- 

 cular reaction. That the essential changes of fat necrosis can 

 be produced postmortem is final proof that they are due to 

 enzymes, rather than to circulatory or cellular action. 



(Arch. klin. Chir., 1906 (78), 845) considers the intoxication of 

 acute pancreatitis as an intoxication with trypsin, which can be checked by 

 antitrypsin. Doberauer (Beitr. klin. Chir., 1906 (48), 456), however, looks 

 upon the products of cellular disintegration as the source of the intoxication. 

 v. Bergmann (Zeit. exp. Path. u. Ther., 1906 (3), 401) states that the toxicity 

 is not due to either the enzymes or to albumoses ; and that it is a true auto- 

 intoxication which can be prevented by previous immunization with either 

 pancreas extracts or commercial trypsin. 



2 Brit. Med. Jour., 1904 (i), 776; Lancet, 1904 (i), 782; 1906, May 19. 



3 Lancet, 1904 (i\ 779. 



*Chiari, Zeit. f. Heilk., 1896 (17), 69; Pforringer, Virchow's Arch., 1899 

 (158), 126; Liepmann, ibid., 1902 (169), 532; Wulff; Berl. klin. Woch., 1902 

 (39), 734. 



