8 Med.-Chir. Trans., vol. xxxv.
9 Ibid., vol. xxvii. p. 162, and vol. xxviii. p. 352.
10 Playfair, A Treatise on the Science and Practice of Midwifery, Philada., 1882.
11 "Embolia dell' Arteria pulmonale," Annali Univers. di Med. e Chir., Milano, 1877–79.
12 De l'Apoplexie pulmonaire, Paris, 1872.
13 Des Embolies veineuses d'Origine traumatique, Paris, 1880.
ETIOLOGY.—The great majority of emboli which are found in the pulmonary artery after death come from the systemic veins. They may also be transferred from the right heart. According to Hayden,14 in fact, the migratory clot is usually derived from cardiac thrombosis of the right heart. This opinion, however, is not generally accepted as correct. Of all the veins of the economy, those of the lower extremities give the largest number of emboli. This statement is notably true of the femoral and internal saphena veins. According to Lancereaux,15 the reason why coagula form in the veins of the lower limbs high up and in the cerebral sinuses is the fact that in these locations the action of the vis-a-tergo and thoracic aspiration is scarcely or at all felt. Besides, we know that coagula of these veins are very frequently found in cachectic conditions (tubercle, cancer) and in the puerperal state (phlegmasia alba dolens). As we shall have reason to remark further on, embolism of the pulmonary artery is often due to fragments of cancer, of pus, of a valve, etc., which have made their way into the return blood-current, or indeed have formed there in the first place. The direct cause of the separation of a portion of thrombus is either some mechanical cause or the influence of regressive changes affecting the clot. We are called upon, however, to consider briefly—1, the causes in a general way which predispose to the formation of thrombi; 2, the diseases, dyscrasic and local, in which emboli occur most frequently. Virchow, Richardson, and others have shown conclusively that the blood is prone to coagulate in the vessels—1, whenever it stagnates or is arrested in its course; 2, if there be, by reason of morbid alteration of vascular wall or presence of an embolus, a mechanical obstacle present; 3, if the blood be modified by septic conditions or increase of fibrin. Now, then, in the veins of the lower extremities we have a considerable tendency to stasis—greater indeed than exists elsewhere in the economy—because these veins have to contend against the weight of the blood in the iliac veins, the venæ cavæ, and the right heart. Further, they are often obliged to resist the effects of accidental pressure in the abdominal cavity, or that which takes place in lungs altered by some chronic diseases16 (emphysema, pneumonia, bronchitis). Usually in these veins, as elsewhere, when a thrombus exists there is local inflammation at its level of the walls of the vein. This inflammatory condition itself is dependent upon mechanical injury, change of the blood (gout),17 or the introduction of septic material. At times septic material is introduced into the blood and absorbs from disintegration of a clot. Hence arise typhoid or pyæmic symptoms.
14 Dis. of the Heart and Aorta, Part ii. p. 1029.
15 Gaz. hébdom., 1862, quoted by Bucquoy.
16 Hayden, Diseases of the Heart and Aorta, Part ii. p. 1023.