Thrombosis and Embolism. 353 



A thrombosis of marasmus has been observed in anaemic and 

 debilitating diseases, and apart from the microbian invasions in a 

 certain number of those affections, this may be looked on as due 

 in part to the lessened density and other changes in the blood and 

 to the debility of the serosa of the vessels. 



The compression of the vascular walls or their penetration by 

 neoplasms, tumors and ulcers, is another cause of coagulation and 

 thrombus, also a varicose or aneurismal dilatation, with weaken- 

 ing of the vascular walls, or dilatation of the heart with structural 

 changes in the endocardium as stated under that heading, or 

 compression of the smaller vessels and capillaries by an exudate 

 in process of organization, or a similar obliteration under the ac- 

 tion of extreme cold. Injury to the serosa of the vessel by 

 stretching, bruising, laceration or section determines a thrombus 

 starting from the injured endothelium. In the smaller vessels 

 the thrombus is usually deep red from the entangling of a large 

 quantity of red globules, whilst in the larger arteries the greater 

 part of the globules pass on and the coagulum is largely buff or 

 straw colored. 



Again in obstruction in the smaller arteries, the inactive capil- 

 lary plexus and the tissue beyond are liable to become gorged with 

 blood with excess of red globules, from the adjacent capillary net- 

 work, constituting infarction, and ending in gangrene. In cases 

 in which this is prevented by the action of intense cold the part 

 may remain pale, as white infarction. 



Causes of Embolism. As already stated embolism results from 

 a detached portion of a thrombus passing to a smaller vessel and 

 obstructing it. Such detachment is favored by molecular softening, 

 liquefaction or suppuration in the clot or beneath it, by the de- 

 structive action of microbes, or by friction or manipulation of the 

 obstructed vessel. Excess of white globules (leukaemia) favors 

 the formation of minute coagula and embolism. Bubbles of air, 

 globules of fat, or cholesterine crystals block the fine pulmonary 

 capillaries, and the debris from atheromatous patches, ulcers, and 

 tumors opening on the inner wall of the artery form emboli in 

 various parts. Finally parasites, especially the larval strongyli 

 in solipedes and filaria and spiroptera in dogs, themselves obstruct 

 the vessels and determine coagulation. 



Pathogenesis. In the larger arteries (aorta, radical stymp of 



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