LIQUEFACTION NECROSIS, CASSATION 319 



coagulins for fibrinogen, it is possible that they also contain coag- 

 ulins for cell-proteids, but this remains to be established. Bacteria 

 produce substances coagulating milk and fibrinogen, and Ruppel l 

 found that the tubercle bacillus produces substances precipitating 

 proteids ; hence coagulation necrosis in bacterial infections may 

 be brought about in this way ; and Schmoll 2 has shown that 

 the necrosis occurring in tubercles is associated with an almost 

 complete coagulation of the cell-proteids. 



Necrosis associated with inflammatory exudation is, of course, 

 accompanied by coagulation of the fibrinogen of the exudate 

 (e. g.j diphtheria) ; this type of coagulation necrosis is chemic- 

 ally a simple fibrin-formation and readily understood. The 

 peculiar hyaline degenerations of parenchymatous cells (e. g., 

 Zenker's degeneration of muscles) are often included under this 

 class, but it would seem more probable that the processes con- 

 sist rather of the fusion of the structural elements of the cell 

 into a homogeneous substance than a true coagulation. No exact 

 data are at hand concerning this point, however. 



I/iquefaction necrosis occurs particularly in the central 

 nervous system, where the cell substance seems not to undergo 

 the coagulative changes described in the preceding paragraphs. 

 Whether this is due to a lack of tissue-coagulins or to a dif- 

 ference in cell composition cannot be said, but the large pro- 

 portion of lipoids in brain tissue is probably an important factor. 

 Probably "edema ex vacuo" is responsible for much of the 

 accumulation of fluid, due to the anatomical conditions that 

 prevent a shrinking or collapse of the tissues to fill in the gap, 

 and the lack of connective- tissue formation. Aseptic softening 

 in general may be safely ascribed to digestion of proteids by 

 cellular enzymes, either from the dead cells or from the leuco- 

 cytes. Suppuration is merely a form of liquefactive necrosis, 

 in which such digestion is particularly rapid because of the 

 large number of leucocytes that are present. Necrosis of the 

 gastric mucosa or of the pancreas is also followed by rapid 

 liquefaction, through the action of the digestive enzymes of 

 these tissues. When necrosis is accompanied by edema (as in 

 superficial burns), the fluid enters the cells in large amounts, 

 presumably because of increased intracellular osmotic pressure, 

 and in this way another form of liquefaction necrosis may be 

 produced. 



Caseation. This term is applied to a form of coagulation 

 necrosis in which the dead tissue has an appearance quite similar 



1 Zeit. physiol. Chem., 1898 (26), 218. 

 2 Deut. Arch. klin. Med., 1904 (81), 163. 



