Part 10

Traumatic thrombi result from a direct injury to the vessel. This may be mechanical, as in the application of ligatures for the obliteration of vessels, the tearing of the veins during childbirth, and the infliction of wounds of every variety. The injury may likewise be chemical, from the action of caustics; somewhat analogous to which, are the effects of heat and cold. Allied to the traumatic thrombi are those which arise {59} from acute inflammation of the intima extending from wounds or inflammatory processes in the vicinity of blood-vessels.

Marantic thrombi are those whose origin is attributable to that enfeebled condition of the body known as marasmus. This represents a weakening of the several functions, especially the circulation, respiration, and locomotion. Such may take place in disease or old age; and it is important to bear in mind those diseases in which marasmus is likely to arise, as thrombosis often proves a complication of such affections. Protracted fevers, as typhus and typhoid, puerperal diseases, the disturbances following surgical operations, chronic wasting diseases, as the tuberculous and scrofulous affections, are all likely to be accompanied by thrombosis. Stagnation of the blood, as well as alterations of the intima, is an important local condition in this variety of thrombosis, which is usually valvular or parietal at the outset, and may be both arterial and venous. Such thrombi are likely to become continued and to serve as a frequent source of embolism.

Thrombi are also divided into primitive, or autochthonous, and secondary varieties. The primitive thrombus is one which owes its local origin to conditions existing at the place of its formation and attachment. The secondary variety demands for its existence a primitive thrombus, whose place of development is remote in time and seat, and from which a part has been transferred to serve as the nucleus for the secondary formation.

The continued thrombus is often confounded with the secondary variety. Continuance is rather a quality of all thrombi, and is essentially growth, whether by lamellation or agglomeration. Such continued thrombi are extended in the course of the circulation, usually by a conical end, which is pointed toward the heart in the case of venous thrombi, but away from this organ when the thrombi are arterial.

Parietal and obstructing thrombi form another subdivision. The former arise from a limited part of the wall of the heart or blood-vessel, and project into its cavity. They are always in contact with flowing blood, and are white or mixed in color and primitive. They may attain a considerable size, and may eventually become obstructing thrombi. The latter are so called when they are of sufficient size to cause a considerable or total obstruction to the current of blood. In the last case the vascular canal is wholly filled by the thrombus. The shape of the older parietal forms is usually globular or pedunculate, owing to the growth in all directions except at the place of attachment; the obstructing thrombi are elongated.

Thrombi are also characterized by consistency and relative absence of moisture. A thrombus is brittle and dry as compared with a clot. In distinguishing between the two, difficulty arises only in the case of a thrombus which may have formed within a few hours before death. Post-mortem clots are moist, elastic, readily withdrawn from blood-vessels, and have a smooth and lustrous surface. Their color is either red, gray, grayish-yellow, or yellow, and is very often mixed. The lighter colors are due to causes which favor the precipitation of red blood-corpuscles before actual clotting takes place, or which occasion an increase of the white blood-corpuscles in fibrin. The thrombus becomes adherent to the vessel wall within a few hours, after its formation, in the case of the red thrombus, and at once, in the case of the white variety. A clot is never adherent, although it may seem so from its entanglement between the trabeculæ and {60} tendons of the heart and the cavernous framework of venous sinuses. Such apparent adhesions are easily recognized by the smooth, shining, intact intima which is disclosed after the removal of a clot.

The thrombus not only tends to become enlarged by further depositions of material from the blood, but it also tends to become diminished in size from the contractile properties of its fibrinous constituent. Moisture is forced from the thrombus in consequence of this shrinkage, and its dryness is increased by subsequent absorption through the wall to which it adheres.

The changes eventually taking place in the thrombus are known as organization, calcification, and softening.

Organization is the transformation of the thrombus into a mass of fibrous tissue. This is accomplished, according to the researches of Baumgarten, by an outgrowth of endothelium from the intima of the vessel, the thrombus being absorbed as the growth of tissue advances. In the case of a thrombus due to the ligation of a vessel, a granulation-tissue also makes its way into the thrombus between the ruptured coats, and the new-formed fibrous tissue which replaces the thrombus becomes vascularized through this granulation-tissue. The vascularization of thrombi surrounded by unbroken walls is most likely to result from the extension into the thickened intima of new-formed branches of the vasa vasorum. Cohnheim claims that the organization of the thrombus may take place solely through the entrance of migratory cells, without any active participation of elements of the vascular wall. The canal is thus obstructed or obliterated by a fibrous tissue, which is pigmented or not, as the pre-existing thrombus contained red blood-corpuscles or not. These, when present, become transformed into granular or crystalline hæmatoidin, which may remain as a permanent constituent of the new-formed tissue.

Even when the thrombus is completely obstructing at the outset, it is not necessary that a total obliteration of the vessel should result from its organization. It not rarely happens, either before or after the thrombus has yielded to the fibrous growth, in consequence of the shrinkage of the fibrin of the thrombus or of the contraction of the fibrous tissue replacing it, that gaps arise which become communicating canals. Through these the blood flows, and the vessel thus becomes only obstructed, not obliterated. The sieve-like tissue thus formed is spoken of as the result of a cavernous or sinus-like transformation of the thrombus. The length of time necessary for the removal of the thrombus and its replacement by fibrous tissue varies considerably. A vascularized granulation-tissue may be present within a week, and in the course of a month the thrombus may have been wholly removed, or a period of months may elapse and the thrombus and granulation-tissue still be present side by side.

The calcification of a thrombus takes place when the latter becomes impregnated with salts of calcium and magnesium. The condition may be present in thrombi which are exposed to a rapidly-flowing arterial stream, as well as in those which lie in venous pockets outside the course of the direct current of blood. The well-known phlebolites are examples of the latter variety. A calcified thrombus may be intimately united to the vascular wall, the results of calcification and organization being associated. Calcification and, in particular, organization represent favorable {61} events in the history of thrombosis, as through their occurrence the process comes to an end, and disturbances, either local or remote, are prevented.

The softening of the thrombus, on the contrary, is always a source of danger. This is partly due to the nature of the products of the softening, whether bland or septic, and partly to the mechanical disturbances produced by the transfer of portions of the softened thrombus to remote parts of the body. All thrombi may become softened. When the process of organization advances normally, the softened parts are absorbed as rapidly as the formation of vascularized fibrous tissue progresses. If this formation is checked or stopped, the process of disintegration still continues. White corpuscles undergo fatty degeneration; red corpuscles give up their coloring matter and become converted, like the fibrin, into granules, and there results a granular detritus. This is present as a viscid, semi-fluid material, either red, gray, or yellow, according to the color of the thrombus. This simple softening is to be regarded as essentially chemical in character, and begins at the oldest portion of the thrombus and advances toward the periphery. Its products are capable of absorption without the production of serious disturbances, and are usually prevented from direct entrance into the blood-vessel containing the thrombus by the continuation of the latter from new coagulation or deposition upon its surface. The thrombus is thus extended as the softening progresses.

When the thrombus is comparatively free from red blood-corpuscles, the softened product, in consequence of its yellowish color, opacity, and viscidity, resembles pus. The so-called encysted abscesses projecting into the cavity of the heart, from its wall, are parietal and globular thrombi, in the interior of which softening has occurred. This form of softening is called simple or bland, as it is free from any evidence of local suppuration, inflammation, or general constitutional disturbance attributable to an absorption of poisonous material.

Septic softening is accompanied by general evidences of a blood-poisoning, and by the local phenomena of purulent inflammation. A suppurative thrombo-phlebitis or arteritis, occurs; that is, an acute inflammation of the wall of the vessel, corresponding in its origin to the seat of the thrombus, and characterized by the formation of pus. In the earliest stage the softened thrombus need not present products differing in appearance from those occurring in simple softening, but their effect is manifested by a rapidly-advancing inflammation of the vascular wall and by the evidence of septicæmia. Inoculation with such material produces a group of symptoms classified under the head of blood-poisoning.

Cohnheim lays special stress upon the presence of micrococci in the softened material, and it is generally agreed that the virulence of septic softening is connected with, if not due to, the presence of microbia. A septic softening may be induced by besmearing, with septic material, the outside of a blood-vessel containing a thrombus, and this form of softening is usually associated with those conditions favoring this relation. Such are the gangrenous wounds following surgical operations, the putrid inflammatory processes affecting the uterine wall after childbirth, the offensive inflammations of the middle ear, and the like. It is possible for a septic softening to occur independently of such contiguous or continuous relations with the surfaces of the body. It is considered, {62} however, that the micrococci present in a softened thrombus must have obtained admission from without through one of the surfaces of the body, mucous or cutaneous, or through undiscovered abrasions of even intact surfaces of peculiar structure, as the alveolar wall or the intestinal mucous membrane. The thrombus is regarded as affording a favorable soil for the growth and activity of the organism.

The mechanical effect of a thrombus varies according to the venous or arterial seat of the same. Venous thrombi, as they are continued toward the heart, tend to become completely obstructing thrombi. In most parts of the body the venous anastomoses are so numerous that the obstruction of a vein is readily compensated for through the collateral venous circulation. When such a compensation is prevented by an extension of the thrombus from branch to branch, and finally to the trunk, an accumulation of blood in the peripheral veins must result. The remote parts become swollen, from the distension of the vessels with blood and the transudation of liquid, and eventually solid material from the blood. Venous thrombosis thus leads to oedema, and even hemorrhage. The more rapidly the obstructing thrombus extends, the earlier and more extreme is the oedema likely to become, while the slower the advance of the thrombus, the more favorable is the opportunity for an enlargement of the collateral vessels through which a sufficient flow of blood is permitted to check oedema and preserve nutrition.

Local mechanical disturbances from arterial thrombi are scarcely perceptible till obstruction is produced, and the results of arterial obstruction will be mentioned in detail in connection with the phenomena of embolism. Cardiac thrombi may occasion local disturbances from interfering with the action of the valves of the heart. Those thrombi which are attached to the valves, especially when calcified, may produce inflammation and aneurism of the opposed wall of the heart, by friction. The most frequent mechanical disturbance from the non-obstructing parietal thrombi of the heart and arteries results from the detachment of fragments and their transfer as emboli to remote parts of the body.

An embolus is a foreign body in a blood-vessel, usually too large to pass through the smallest capillaries, and the disturbances resulting from its presence are included under the term embolism. Although most emboli are detached portions of thrombi, any foreign body of suitable size may become an embolus. Such are tissues, as the pulmonary elastic fibres, fragments of diseased valves of the heart and of the intima of arteries, or portions of tumors growing into vascular canals. Others are globules of oil entering the torn veins when fat-tissue becomes crushed, or air-bubbles admitted through veins either wounded by instruments or opened after parturition by the dislodgment of their obstructing thrombi. Still others are granules of pigment derived from the coloring-matter of the blood, as in melanæmia, or introduced from without, as india-ink and cinnabar. The echinococcus has been found as an embolus, and it is highly probable that the cysticercus, the trichina, and other animal parasites may be disseminated as emboli over the body.

Vegetable parasites, like the bacterium and aspergillus, have also been included in the list, although the disturbances resulting from their presence are less due to mechanical obstruction than to colonization and growth. The experimenter uses the most various objects as emboli--bits {63} of wood, rubber, and glass, globules of mercury, fragments of tissue, etc. Emboli are to be regarded as of arterial or venous origin. The arterial emboli are carried toward the capillaries, while venous emboli are carried toward the heart. The effect of both is partly or wholly mechanical, and partly due to the specific properties of the constituents.

The mechanical effect of an embolus is manifested by the obstruction it offers to the circulation, and the degree of the obstruction depends upon the size, shape, and density of the embolus and the nature and size of the vessel obstructed. An embolus may be so large as to be unable to pass through the valvular orifices of the heart. A long and narrow embolus might pass through a vessel which would not admit one which was short and thick. A jagged and dense embolus, by repeated blows or prolonged and forcible contact, might cause a weakening or rupture of the wall of a vessel, and thus produce an aneurism. Certain vessels (the terminal arteries of Cohnheim) furnish the sole supply of arterial blood to a district, and when they are obstructed, the results, to be mentioned later, differ widely from those taking place where free vascular anastomoses exist. When a trunk bifurcates, the larger branch usually receives the embolus.

Venous emboli are those which approach the heart by the peripheral veins of the body or the pulmonary veins, and the liver by the radicles of the portal vein. Emboli from the veins of the body are carried through the right side of the heart, if not so large as to be stopped at the tricuspid or pulmonary opening. As they enter the latter, they are carried along its course under the influence of gravity and the direction and force of the current, which are determined by the direction and relative size of the bifurcations of the artery, the right primary branch being larger than the left. Eventually, a point of the artery is reached whose diameter is less than that of the embolus, and the latter is stopped. This point usually corresponds with a place of bifurcation, and the embolus frequently rides the wall separating the branches.

Emboli from the radicles of the portal vein owe their most frequent origin to thrombi associated with inflammatory processes in the intestine, especially of the cæcum and vermiform appendage, to inflammatory processes in the spleen and obstruction to the flow of blood through the splenic artery, or to inflammatory changes proceeding from the kidneys. Such venous emboli are carried toward the heart, but are stopped on the way by the intrahepatic branches of the portal vein.

Arterial emboli are those which enter the left side of the heart from the lungs, which arise in the left ventricle or auricle, which may pass through an open foramen ovale from the right auricle, or which arise from the arterial wall. They are carried along the course of the arterial circulation, and are distributed over the different regions and organs of the body. Usually following the more direct course of the circulation, they are more likely to enter the abdominal aorta than to be carried toward the brain or upper extremities. Embolism of the carotids, especially of the left carotid, is more likely to ensue than embolism of the subclavians. Embolism of the coronary arteries is rare, while embolism of the splenic artery, the left renal and left iliac arteries, is comparatively common, and in the order mentioned.

When an embolus is found, or embolism suspected, the source is always {64} to be searched for in those regions from which the affected part receives its blood. The source of arterial and portal emboli is usually found with ease, while the pulmonary embolus may come from so wide a region, the body-veins, that much time may be spent before its place of origin is discovered. An appreciation of the laws of the transfer of emboli renders such a discovery almost certain.

When the embolus reaches a point beyond which it cannot pass, the resulting disturbance depends essentially, as shown by Cohnheim, upon the presence or absence of arterial anastomoses beyond the place of obstruction. He gives the name terminal arteries to those which have no anastomosing arterial branches. These are met with in the spleen, kidneys, lungs, brain, and retina. If the obstructed artery is not terminal, the embolus may produce no further disturbance, the collateral supply of blood through the anastomoses sufficing for the nutrition and function of the part. If, however, the vessel is a terminal artery, and the embolus is completely obstructing, the supply of arterial blood must be wholly cut off from the region beyond the seat of obstruction.

If the embolus does not completely obstruct at once, it soon becomes sufficiently large for this result to ensue in consequence of a secondary coagulation. The rider assumes legs extending into the arterial branches beyond the place of obstruction, and a body which extends backward in the course of the circulation to the nearest branch. The result of the total obstruction of the vessel is to cut off the admission of arterial blood, producing a local anæmia. The contraction of the elastic tissues of the part propels toward the capillaries a certain quantity of the blood in the vessels beyond the point of obstruction, till this force becomes neutralized by the blood-pressure in the vessels surrounding the obstructed region. The anæmic part may subsequently become engorged with blood; it may die, a region of anæmic necrosis resulting, or the dead portion may become softened.

The engorgement of the obstructed territory has received the name of hemorrhagic infarction. A solid, wedge-shaped mass of a reddish-brown color is present, whose shape is due to the arborescent branching of the terminal arteries. According to Cohnheim, the engorgement of the region with blood takes place from venous regurgitation into the obstructed part, till the intravenous pressure is overcome by the resistance of the tissues in the region affected. The capillaries and larger vessels thus become distended, and an escape of liquid and solid constituents of the blood takes place. If the veins are provided with valves, or the venous regurgitant current is opposed by gravity, the hemorrhagic infarction is prevented or greatly impeded.

Litten, on the contrary, who has furnished a recent contribution to this subject, claims that the hemorrhagic results of embolism are not accomplished through venous regurgitation, unless increased venous tension is produced by coughing, vomiting, and like efforts. His experiments lead him to maintain that arterial blood from surrounding tissues is supplied to the obstructed region through the anastomosing capillaries. The force is not sufficient to drive the blood through the capillaries into the veins beyond, but an accumulation takes place in the capillaries, which become dilated and distended. The escape of blood-corpuscles and {65} serum then takes place, the more freely, as Weigert suggests, the larger and more numerous are the pre-existing spaces in the organ. Hence the infarction becomes the most characteristically developed in such organs as the lungs and spleen. Causes which obstruct the venous flow, as well as those which increase the arterial tension, promote the hemorrhagic infarction.