Thrombosis and Embolism. 491 



endothelium sets free the so-called fibrine ferment, and precipi- 

 tates coagulation. leister found that contact of ammonia with 

 the interior of an otherwise living vein caused a thrombus. So in 

 all endarteritis and phlebitis coagulation takes place on the serosa 

 and quickly blocks the vessel. Even in the capillary vessels the 

 same principle holds, and in inflammation minute coagula 

 (thrombi) form in the capillary network throughout the whole 

 inflamed area. This explains not only the capillary blood stasis 

 but the thrombosis of inflamed arteries and veins. In these two 

 latter the clot increases and extends in the direction of blood 

 stasis : — in the artery toward the heart as far as the next collateral 

 branch, and in the veins away from the heart as far as to the 

 next collateral trunk. On the distal side of the arterial throm- 

 bus the blood flows off freely toward the capillaries, but on the 

 proximal or cardiac side it is absolutely stagnant up to the next 

 branch through which it can freely flow into the capillary plexus. 

 Into this stagnant blood the fibrine ferment, produced by the 

 altered white globules in the clot already formed, slowly extends 

 until the whole has formed a firm coagulum. Beyond this the 

 actively rtioving blood carries off and dilutes this ferment so 

 rapidly that it can exert no appreciable effect on the fibrine- 

 forming elements. The principle is an important one in sur- 

 gery, as the clot formed entad of the ligature will be extensive 

 in proportion to the distance from the first collateral trunk, and 

 in inverse proportion to this clot will be the danger of second- 

 ary haemorrhage. In veins the same rule holds, with this differ- 

 ence, that as the blood is flowing toward the heart it empties the 

 vessel on the cardiac side, and stagnates on the distal side up to 

 the next collateral branch. Hence it is that a thrombus in a 

 vein always extends away from the heart, while that of the 

 artery extends toward it. 



Another cause of coagulation is the deoxidation of the blood 

 and the excess of carbon dioxide. This occurs in the stagnant 

 blood in the vessels and above all in the capillaries. The normal 

 trophic changes in the serosa, fail to take place in contact with 

 blood in this state, and the resulting changes in the white and 

 endothelial cells set free fibrine ferment and determine coagula- 

 tion. Stasis of the blood from any cause (ligature, pressure, em- 

 bolism) tends to this condition and the extension of the coagulum. 



A thrombosis of marasmus has been observed in anaemic and 



