322 DISTUh'BAXCES OF CIRCULATION 



coagulability is not constantly if at all alteral by fever, cancer, dia- 

 betes, slight secondary anemias, or many other diseases, and in nor- 

 mal conditions it remains fairly constant. In infants the coagulation 

 time is slightly shorter than in adults. The coagulation is hastened 

 after considei-able hemorrhages, in endocarditis, and perhaps in aneu- 

 rism and thrombosis ; and is commonl}- delaj'ed in the acute exan- 

 themata, in hemophilia, in purpura neonatorum, and occasionally in 

 some other diseases.'* There is entire lack of agreement concerning 

 the reputed acceleration of coag'ulation by oral administration of cal- 

 cium salts, and retardation by citrates; and the supposed thrombo- 

 plastic influence of gelatin cannot be shown consistently by direct ob- 

 servations. In jaundice, calcium salts probably have an effect, since 

 here the cause of the deficient coagulation seems to be the fixation or 

 precipitation of the blood calcium by the bile pigments. It seems 

 probable that the measurement of the time required for coagulation to 

 take place in vitro does not exactly represent the tendency of the same 

 blood to coagulate in the body of the person from whom it is obtained ; 

 for example, the injection of foreign serum has a notable effect in stop- 

 ping hemorrhages, but the coagulation time of the recipient's blood is 

 not correspondingly altered. Whipple's observations that with a low 

 fibrinogen content the blood may coagulate in normal time, and yet the 

 clots be too delicate to stop hemorrhage, explains at least part of the 

 discrepancy; and of similar significance is the fact that with a very 

 low platelet count the blood may coagulate a.s rapidly as normal, but 

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

 vere purpura hemorrhagica we may have a normal clotting time. 

 In other conditions with normal coagulability, hemorrhages may re- 

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

 cially in hepatic diseases.'^'*^ 



THE FORMATION OF THROMBI 



If we apply the facts brought out in the precetling 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, 



54 See Dochez, (.Jour. Exp. MckI., 1912 (16), 69:?), wlio found s.mic delay in 

 coagulation in pneumonia. Corroborated by Minot and l.cc, .lour. Aiiur. ^led. 

 Assof.. 1917 (6S), 545. 



5411 See (ioodpasture. Bull. .Johns Hopkins Hosj)., 1914 (25). :?30. 



•>^> Albutt's System, vol. (!, complete (liscusaion of the {general featuri's of throm- 

 bosis; also see Kiister, P^rpeb. inn. IMed., 1913 (12), 667; Zurhelle, Ziejrler's 

 Beitriifie, 1910 (47), 5.39; Sdiwalbe, Krfjebnisse Pathol. . 1907 (XI (2) ). 901; 

 I..ubar8ch, All<r. Pathol., Vol. 1, Wiesbaden. 1905. Also see Asehofl'. Ziegler's 

 Beitr., 1912 (.52), 205. and Arch. Int. Med., 191;? (12), 50.1, eoneerninji the 

 mechanics of thrombus formation. 



