THROMBOSIS 323 



low platelet count the blood may coaguhite as rapidly as normal, but 

 the clots do not shrink and become firm (Duke). Hence with a se- 

 vere purpura hemorrhagica wc may have a normal clotting time. 

 In other conditions with normal coagulability, hemorrhages may re- 

 sult from excessive fibrinolysis which causes solution ol" the clot, espe- 

 cially in hepatic diseases. ^ 



The Formation of Thrombi 



If we apply the facts brought out in the preceding discussion rela- 

 tive to the factors in the coagulation of blood, to the manner and 

 conditions under which thrombi are formed in the circulating blood, 

 we find explanations for many of the features of thrombosis. Welch^ 

 describes the steps in the formation of a thrombus after injury to the 

 vessel-wall, as follows: First, there is an accumulation of blood- 

 platelets adhering to the wall at the point of injury. Leucocytes, 

 which may be present in small numbers at the beginning, rapidly in- 

 crease in number, collecting at the margins of the platelet masses and 

 between them. Not until the leucocytes have accumulated does the 

 fibrin appear. As Welch remarks, these findings afford no conclusive 

 evidence as to whether fibrin-ferment is formed from the leucocj'tes 

 or from the platelets, but since the fibrin does not appear until after 

 the leucocytes have accumulated, and also since small thrombi may 

 consist solely of platelets without fibrin, it seems probable that the 

 leucocytes must be looked upon as the chief source of the ferment. 

 If the blood is made incoagulable by injection of hirudin, injury to 

 the vessel-walls causes the formation of thrombi composed entirely of 

 platelets (Schwalbe). Sometimes small clots may form without the 

 apparent participation of either platelets or leucocytes. These purely 

 fibrinous thrombi seem to start from injured endothelial cells, par- 

 ticularly in inflammatory conditions, such as pneumonic lungs, and 

 give the impression that the coagulin is derived from the endothelial 

 cells. Zurhelle attributes by far the most important part to the 

 platelets, an opinion shared by many, including Derewenko,'* who 

 holds that the coagulation of' blood with entirelj^ occluded vessels is 

 quite distinct from true thrombosis because of the lack of platelets 

 in stagnant blood. ^ Clots formed in the absence of platelets do not 

 shrink like proper thrombi (Duke). 



The process of clotting in the stoppage of hemorrhage offers some 



2 See Goodpasture, Bull. Johns Hopkins Hosp., 1914 (25), 330. 



^ Albutt's System, vol. 6, complete discussion of the general features of throm- 

 bosis; also see Kiister, Ergeb. inn. Med., 1913 (12), 667; Zurhelle, Ziegler's Beitrage, 

 1910 (47), 539; Schwalbe, Ergebnisse Pathol., 1907 (XI (2) ) 901; Lubarsch, 

 AUg. Pathol., Vol. 1, Wiesbaden. 1905. See Aschoff, Ziegler's Beitr., 1912 (52), 

 205, and Arch. Int. Med., 1913 (12), 503, concerning the mechanics of thrombus 

 formation. 



* Ziegler's Beitr., 1910 (48), 123. 



^ Not accepted by Schwalbe, loc. cit.^ 



