114 THE BLOOD AND THE LYMPH 



blood vessels and by disintegrating shed forth prothrombin and thrombo- 

 plastin, that the clotting starts. This platelet agglutination may result 

 from stagnation in the bloodflow, or from roughening and damage to the 

 vessel walls. Stagnation may be due either to failure of the circulation 

 as a whole as in heart disease, or to local physical alterations in the vas- 

 cular tube, setting up conditions in which eddy currents with stagnant 

 pools of blood are formed, such as will occur at places where the vessels 

 suddenly become wider, as in varicose veins, in aneurisms and at the 

 sudden bend of large veins. The first formed (platelet) thrombus is fol- 

 lowed by one of a darker color, which fills the vessel up to the next 

 anastomotic branch. Similar stagnation may also follow the obstruc- 

 tion caused by lodgment of emboli in the smaller vessels (air, foreign 

 bodies in fine suspension, bacteria, etc.). The thrombi in such cases are 

 very small and occur particularly in the capillaries of the liver, spleen, 

 and lungs. The small thrombi often serve as foci from which clotting 

 spreads into the larger vessels, this being often encouraged by an increase 

 in the coagulability of the blood. When the intima is inflamed, it is pos- 

 sible that excessive amounts of thromboplastin are produced and that 

 this neutralizes the antithrombin in blood moving so slowly that it is not 

 replaced by fresh blood before clotting ensues, or it may be that sub- 

 stances derived from the inflamed tissue cause the platelets to aggluti- 

 nate. The increased clotting often observed after the injection of hemo- 

 lytic agencies (foreign sera, snake venom, etc.) may also be due to 

 platelet agglutination. Like the thrombosis following embolism, the 

 clotting occurs at first in the capillaries, the initial thrombi containing 

 masses of platelets along with skeletons of blood corpuscles and cells 

 from the blood-forming organs. 



