Embolism is the blocking of a bloodvessel by a clot or other solid body formed at a distant point of the circulation floated on in the blood stream, and arrested when it reaches a vessel too small to transmit it.
A thrombus may be formed at any point of the circulatory apparatus (heart, arteries, veins) whenever the conditions are such as to determine coagulation of the blood. An embolism on the contrary is a disease of the arteries since in these the blood current, proceeding centrifugally from the greater to the lesser, inevitably carries the moving solid to a point too narrow to allow of its further progress. Thus clots originating in the systemic veins or right heart pass to the lungs and produce embolism of the pulmonary arteries whereas those formed in the pulmonary vein or left heart are arrested in some part of the systemic arteries. Clots formed in the portal vein however are arrested in the hepatic vessels into which that trunk breaks up.
Causes of Thrombus. The production of a thrombus may be due to the condition of the blood or of the vessels. The researches of Buchanan, Schmidt, Hammersten and others show that two albuminoid elements, fibrinogen and paraglobulin, present in the living blood, and a fibrine ferment mainly derived from the white corpuscles in process of change or destruction, determine powerfully the formation of fibrine and clot. Hewson, Brücke and Lister have shown that blood may be maintained fluid for many hours in an unimpaired vein, or turtle’s heart though it may have been removed from the body, the important condition being that the vein shall retain its vitality and suffer no derangement of its endothelium. Lister has even shown that blood may remain fluid for many hours in a sterilized glass tube which has been filled by passing the tube carefully into such a vein without disturbing its lining membrane, or imparting motion to the liquid. In such a case a thin film of coagulum only, forms on the interior of the glass tube. In healthy blood, without addition of any extraneous matter, and kept perfectly still, the plasma and globules retain their integrity, and the former its fluidity for a length of time. But if shed into a basin it coagulates at once.
a. Changes in the blood. Contact with foreign bodies generally determines this change and prompt coagulation. Transfixing the artery with a needle, even a silver one, the entrance of parasites (actinomycosis, strongyli, filaria), the presence of pus, and of certain infectious microbes and their products, the introduction of solid particles and even of air into the vessels, the transfusion of blood which has been exposed to receive ærial germs, or which contains microscopic clots, or the globules of which have become modified by contact with a basin or other vessel, even the transfusion of defibrinated blood may cause coagulation. The danger is always greater if the blood is drawn from a different genus and unfitted to live in the blood of the recipient. Disease germs are especially dangerous if adapted to colonize the serosa of the vessel and destroy its epithelium. A decrease of the density of the blood favors coagulation, a lowering of one thousandth rendering it syrupy, and various chemical agents induce or favor coagulation, thus acetic acid, valerianic acid, alcohol, the salts of iron, and above all the salts of lime act in this way. Very high and low temperatures throw down the fibrine as a grumous precipitate, but the clot remains soft.
b. Changes in the vessels. Any disturbance or alteration of the endothelium sets free the so-called fibrine ferment, and precipitates coagulation. Lister found that contact of ammonia with the interior of an otherwise living vein caused a thrombus. So in all endarteritis and phlebitis coagulation takes place on the serosa and quickly blocks the vessel. Even in the capillary vessels the same principle holds, and in inflammation minute coagula (thrombi) form in the capillary network throughout the whole inflamed area. This explains not only the capillary blood stasis but the thrombosis of inflamed arteries and veins. In these two latter the clot increases and extends in the direction of blood stasis:—in the artery toward the heart as far as the next colateral branch, and in the veins away from the heart as far as to the next colateral trunk. On the distal side of the arterial thrombus the blood flows off freely toward the capillaries, but on the proximal or cardiac side it is absolutely stagnant up to the next branch through which it can freely flow into the capillary plexus. Into this stagnant blood the fibrine ferment, produced by the altered white globules in the clot already formed, slowly extends until the whole has formed a firm coagulum. Beyond this the actively moving blood carries off and dilutes this ferment so rapidly that it can exert no appreciable effect on the fibrine-forming elements. The principle is an important one in surgery, as the clot formed entad of the ligature will be extensive in proportion to the distance from the first colateral trunk, and in inverse proportion to this clot will be the danger of secondary hæmorrhage. In veins the same rule holds, with this difference that as the blood is flowing toward the heart it empties the vessel on the cardiac side, and stagnates on the distal side up to the next colateral branch. Hence it is that a thrombus in a vein always extends away from the heart, while that of the artery extends toward it.
Another cause of coagulation is the deoxidation of the blood and the excess of carbon dioxide. This occurs in the stagnant blood in the vessels and above all in the capillaries. The normal trophic changes in the serosa, fail to take place in contact with blood in this state, and the resulting changes in the white and endothelial cells set free fibrine ferment and determine coagulation. Stasis of the blood from any cause (ligature, pressure, embolism), tends to this condition and the extension of the coagulum.
A thrombosis of marasmus has been observed in anæmic 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 weakening 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 action 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 capillary plexus and the tissue beyond are liable to become gorged with blood with excess of red globules, from the adjacent capillary network, 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 destructive action of microbes, or by friction or manipulation of the obstructed vessel. Excess of white globules (leukæmia) 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.