THE HEMORRHAGIC DIATHESIS 139 



would of course be that there was some unused 

 thrombin present as well, too much having been added 

 to the fibrinogen.) 



Thus, the exact pathology of haemophilia would be, 

 in Addis's opinion, a congenital defect in the con- 

 stitution of the prothrombin, whereby it yields 

 thrombin much too slowly. Possibl}^ the leucocytes 

 are ultimately at fault. 



The practical deduction we shall see later. 



5. There is no excess of antithrotnbin in the plasma 

 of the bleeder. If there were, the addition of a trace 

 of normal blood would not cause haemophiliac blood 

 to clot as it does, because any thrombin in the former 

 would be overpowered and destroyed by the anti- 

 thrombin in the latter. 



To sum up, the secret of haemophilia lies in a 

 defective quahty of the prothrombin, such that it 

 takes much longer than usual to develop into 

 thrombin. No evidence is yet to hand to show 

 whether the haemorrhagic tendencies in scurvy, 

 purpura, pernicious anaemia, and occasionally in 

 jaundice have the same explanation. 



It is important to bear in mind the fact that 

 certain cases of jaundice may ooze to death by 

 capillary haemorrhage after operation ; most of us 

 can recollect instances of this calamity. It has been 

 recommended to give drachm doses of calcium 

 chloride for three days before the operation, but 

 probably a more useful proceeding would be to take 

 the coagulation time by means of a Wright's tube, 

 and to refuse to operate on any cases showing serious 

 delay. 



