In most cases of thrombosis there is either a stagnation of the blood or else some palpable injury to the vessel compromising its endothelium, and the various thrombi may be studied according as they are formed in one of these ways or the other, while in some cases the action of both may be traced. As we have already seen, the stagnation is rarely complete, and accordingly the thrombi are mostly white or mixed, being formed in the way just described.

(A) Thrombosis From Stagnation Of Blood

It will be found that wherever the circulation is so altered that, while the blood moves more or less freely in the general current, there are subsidiary currents or eddies, thrombosis is liable to begin in the situation of the latter.

Fig. 26. - Thrombus in auricle of heart. The muscular tissue of the heart is shown in longitudinal and transverse section, and, lining it, the endocardium. The thrombus bulges out from a recess, x 4:2.

Local dilatations produce this very directly. In cases of aneurysm or varix there is a pouch containing blood which is out of the regular current and thrombosis is liable to occur, although in the case of aneurysm there is the additional fact that the wall is considerably altered. Weakness of the heart, especially when associated with dilatation, leads to imperfect emptying of its cavities, and the blood forms eddies in the parts most removed from the general current (see Fig. 26). White thrombi often form in this way behind the columnse carnese, in the auricular appendages, and near the apices of the ventricles. These thrombi often assume a globular shape (Globular vegetations of Lsennec), and may grow to a large size. General weakness or marasmus, occurring in consequence of debilitating diseases, such as typhoid fever, phthisis, etc., renders the current in the veins sluggish. There is under these circumstances not only weakness of the heart, but the muscles being weak do not assist in emptying the veins, and 'respiration also fails to give due assistance. While there is a general sluggishness, the localities in which the thrombosis begins usually correspond with bye currents in the circulation. The blood in the veins moving slowly and at a low pressure does not press back the valves against the walls of the veins. Hence as the valves are half open, the blood will stagnate in the sinuses of the valves, and thrombosis is liable to occur there. Coagula so formed grow up the veins, but even when they are continuous they usually present a knotted character from the parts corresponding with the valves being bulkier. This knotted condition is sometimes detectable through the skin. Again marasmic thrombi often begin in the longitudinal sinus of the dura mater. This vessel has somewhat rigid walls, and the tributary veins from the pia mater are small, and in the erect posture the blood passes upwards to the sinus against the force of gravitation. If the current in the veins be slow then there will be eddies in the sinus, especially at the parts lying highest. The most common starting point is indeed the highest part of the sinus (Recklinghausen). Thrombosis in the uterine veins after delivery is partly due to stagnation of blood in cases where the uterus contracts imperfectly, but the injury to the veins in the removal of the placenta contributes.

(B) Thrombosis From Alteration Of The Wall

Wounds of vessels induce thrombosis, and this process bears an important part in stilling haemorrhage. If the blood is stagnating in the veins, as is the case in passive hyperemia from heart disease, a trivial wound may start a thrombosis. Thus, in cases of valvular disease the legs are not infrequently punctured to relieve the oedema which is so common in such cases, and the punctures may be the starting points of thrombosis. Ligature of vessels causes thrombosis, as there is rupture of the internal and middle coats. Acute inflammation of the walls of the heart or vessels induces coagulation, as one sees so frequently in acute endocarditis. Chronic endocarditis and atheroma, by producing palpable alterations in the endocardium or internal coat of arteries, are frequent causes of thrombosis, more particularly when calcareous matter is deposited and becomes exposed to the blood. An occasional cause is the protrusion of tumours through the walls of vessels, but this scarcely ever occurs in arteries and is rare in veins.

(c) There are cases in which coagulation occurs apparently in consequence of the sudden setting free of the ferment in the general circulation. This has been mostly in cases of transfusion, where blood from one of the lower animals has been used. (See case by Recklinghausen).

It is important to distinguish Thrombi which have formed during life from mere Post-mortem Coagula. It will be clear from what has gone before that the thrombi are mostly either white or grey, but being formed largely of white corpuscles they are of a dead or opaque white or grey appearance. Post-mortem clots are sometimes pale from the sinking of the red corpuscles or otherwise, but they are gelatinous and smooth on the surface and mostly translucent, whereas the thrombi are firmer, drier, more opaque and granular on the surface. The thrombi also adhere to the wall to some extent, whereas the clots do not, although in the heart, from getting entangled among the columnse carnese, they may have an appearance of adhesion. Lastly, the thrombi are often stratified, indicating their deposition in successive layers.

Growth Of Thrombi

Thrombi begin as local depositions on the internal surface, but they are liable to grow till they may fill the vessel, obstructing it and extending to further portions of the vessel. The thrombus is composed of dead matter, and its surface is rough, so that the conditions are given for further deposition, unless the current is rapid. The influence of the blood-current in determining the extension of thrombosis is well shown in the case of ligature or severance of arteries as in amputations. The accompanying illustra tion (Fig. 27) shows a section of a small artery from a stump. It was not ligatured, but its mouth is filled with a thrombus which extends 'exactly to the first branch proximal to the plug, or to the point where the circulation becomes active. In the case of the veins the blood will be for the most part stagnant above and very often below the thrombus, and it is in these vessels particularly that thrombi are apt to grow very extensively. Thus a coagulation starting in the uterus may travel along to the internal and common iliac veins, and thence pass into the veins of the legs. In a case observed by the author, coagulation had its origin in a cancer of the kidney which involved the walls of the renal vein; it extended thence to the inferior vena cava, and to the veins of both legs which were distended with old thrombi. Thrombi in the veins will often be found growing on till they reach a vessel where the circulation is very free, and the globular thrombi in the heart often grow so as to project into the cavity. Growing thrombi will be mostly white or mixed, but as the blood above and beneath an obstructing thrombus is usually at a stand-still or nearly so, they may be almost purely red in parts.

Fig. 27. - Section of a small artery from a stump. The bleeding has been stopped by a thrombus without ligature. The thrombus conies accurately to the level of a branch going off to the right, x 6.

Before leaving this subject, it may be well to consider Whether thrombosis occurs in the living capillaries. It is to be remembered that, so long as the living endothelium exercises its due influence on the blood, coagulation will not occur. As the capillary wall is entirely composed of flat cells, it is only when necrosis takes place that the conditions requisite for coagulation will be fulfilled. Moreover, as the tissues depend on the capillaries for their nutrition, obstruction by thrombosis will involve the death of the tissues themselves. Hence thrombosis of the capillaries, or even complete stagnation in them, may be put out of the question except in connection with necrosis. If this were not so, the thrombi in veins would grow into the capillaries, and, through them, into the arteries. The capillaries, not admitting of this, form a barrier to the extension of the coagulation. It thus happens that, after extensive coagulation in the veins, the circulation is largely maintained by arteries, capillaries, and lymphatics, and necrosis rarely occurs. It is worthy of note in connection with this matter that the blood found in the capillaries after death is nearly always fluid.