THE H.EMORRHAGIC DIATHESIS 137 



we are to blame of the various elements that take 

 part in regulating the coagulation of the blood, the 

 problem becomes complicated. 



Theoretically, the delay might be due to : — 

 (i) Deficient quantity or quahty of the fibrinogen ; 

 (2) Deficiency or excess of calcium salts ; (3) De- 

 ficient quantity or quality of the thrombokinase ; 



(4) Deficient quantity or quahty of the prothrombin ; 



(5) Excess of antithrombin. 



In the examination of these factors we follow the 

 researches of Addis. The main point to determine 

 is whether the delay is in the first or the second of 

 the two reactions involved, — that is, in the conversion 

 of prothrombin into thrombin, or in the conversion 

 of fibrinogen into fibrin. It proves that the former 

 is at fault ; the latter is quite normal. HsemophiUac 

 fibrinogen is as readily clotted by normal or by 

 haemophiliac thrombin as is normal fibrinogen, and 

 normal fibrinogen is easily clotted by thrombin from 

 a bleeder. But the hsmophihac blood must stand 

 a long time before any prothrombin is converted into 

 thrombin. 



Taking up the points, then, in order : — 



1. TJw defect is not in the fibrinogen, because it 

 is readily clotted if isolated and treated with throm- 

 bin. Moreover, when clot does at last form during 

 a haemorrhage, it is as firm and abundant as in 

 ordinary blood. 



2. The defect is not in the calcium salts, because 

 analysis shows no abnomiahty in quantity, and the 

 addition of these salts to drawn haemophiUac blood, 

 though it may hasten the time of clotting, does not 

 bring it to normal. 



