EMIiOLISU 325 



called " fih rin- ferment ihromhosis," tlie lliroinl)! are merely agglu- 

 tinative thrombi, devoid of fibrin ; this is undoubtedly true for many 

 of the thrombi observed after poisoning with the ]iowerfn1Iy agglutin- 

 ative snake venoms (see Chap. vi.). Bacterial hemagglutinins may 

 also cause the formation of hyalin thrombi.*''' On the other hand, 

 some, at least, of the hyalin capillary thrombi are undoubtedly com- 

 posed of soft masses of fibrin which have not become fibrillar, al- 

 though the successful staining by fibrin stain is not final proof of the 

 fibrinous nature of a thrombus. The liver necrosis which follows ether 

 injections in animals is caused by fibrinous thrombi which result from 

 liberation of coagulins by the injured cells (L. Loeb). 



Secondary Changes in Thrombi. — The changes that occur in 

 thrombi after they have existed for some time are largely due either 

 to ingroA^i;li of new tissue or to calcification, the latter of which will 

 be considered in a separate chapter. The only other change of inter- 

 est from the chemical standpoint is the central softening which may 

 occur in any large thrombus, but is particularly often observed in the 

 large globular thrombi found in the heart. The center of the throm- 

 bus may be so completely softened that it resembles a sac of pus, the 

 contents, according to Welch, consisting of necrotic fatty leucocytes, 

 albuminous and fatty granules, blood-pigment and altered red corpus- 

 cles, and occasionally acicular crystals of fatty acids. Undoubtedly 

 this softening is related to the process of fibrinolysis previously de- 

 scribed, and depends upon digestion of the fibrin by leucocytic en- 

 JijTnes,®* but the fact that the central portion alone undergoes soften- 

 ing is of interest, suggesting that the antibodies for leucocytic pro- 

 teases, which Opie ^'^ found present in normal serum, prevent digestion 

 at the surface of the clot. The same fact indicates that the tissue 

 fibrinolysins ^^^ do not plaj' an active part in softening clots. 



EMBOLISM 



Emboli offer little of chemical interest, because of the purely me- 

 chanical nature of their origin and of the effects they produce.®*^ An 

 exception exists in the case of fat emholism, for the manner in which 

 the fat is removed from the blood has invited considerable specula- 

 tion."' Part of the fat is eliminated in the urine, "'^ but the problem 

 of how it escapes from the glomerular capillaries is not satisfactorily 

 explained ; large emboli undoubtedly lead to rupture of the capillary 

 walls, and probably some fat also escapes through stomata or similar 



63 Pearce and Wiiine, Amer. Jour. Med. Sci.. Oct., 1904. 



64 Barker, Jour. Exp. ]\[od., Ifl08 (10), 343. 



65 Jour. Exper. Med.. 190.5 (7), 316. 



65a See Fleisher and Loeb. Jour. Biol. Chem., 1915 (21), 477. 



66 Fat embolism mav follow poisoning with potassium chlorate (Winosradow, 

 Virchow's Arch., 1907 "( 190) . 92) . 



67 Full discussion by Beneke, Ziegler's Beitr., 1897 (22). 343. 



67a Discussed by Sakaguchi, (Biochem. Zeit., 1913 (48), 1) who finds a little 

 fat in the normal urine. 



