This section is from the book "A Manual Of Pathology", by Joseph Coats, Lewis K. Sutherland. Also available from Amazon: A Manual Of Pathology.
If a thrombus contains red corpuscles, then their colouring matter is soon dissolved out and stains the coagulum, giving it frequently a deep brown tint. The pigment sometimes deposits crystals of hsematoidin, which may remain long unaltered. (See Fig. 28.) In course of time further changes occur, of which the more important are softening and organization.
Softening is a frequent result, especially in the coagula in the heart and veins. The globular thrombi in the heart frequently exhibit this process. It begins in the central parts of the thrombus, and the coagulum breaks down into a turbid brownish juice, the softening extending gradually outwards. The juice is often like a mixture of pus and blood, or in very white thrombi it may be like pure pus. It consists of the debris of the thrombus, and no well preserved corpuscles are to be found in it. The softening may extend outwards till a mere rind is left, and this may give way and cause the juice to be launched into the circulation. Another form of softening is that which occurs in thrombosis due to septic infection, in the condition known as Thrombo-phlebitis. Thrombi, instead of softening, may dry in and shrivel. In such case we may have lime salts deposited, and even, through time, the formation of little stony masses - Vein-stones or Phleboliths.

Fig. 28. - Crystals of hasmatoidin found closely aggregated in the midst of an old thrombus in a vein. The crystals have a deep red colour, x 350.

Fig. 29. - Section of carotid artery in which a thrombus is completely replaced by connective tissue. The sections of many vessels are shown, x 12.
The Organization and Absorption of a thrombus is a process of some interest. As the coagulum is dead, it is clear that it cannot take part in the process of organization. In studying inflammation this subject will come up for fuller discussion, but it may here be stated that when a piece of dead animal substance is present among the living tissues, the first step towards its absorption is usually its replacement by an elementary tissue, the dead structure constituting, as it were, a mould on which the new tissue forms itself. In the case of the thrombus new-formed tissue springs from the wall of the vessel, and this is accompanied by vessels which sprout from those of the vessel-wall. A vascular tissue thus by slow degrees eats into and replaces the blood-clot. Through time the calibre of the vessel is occupied by vascular connective tissue as in Fig. 29. This may shrink and obliterate the calibre of the vessel. But sometimes, especially in veins, there occurs a process which is shown in Figs. 29 and 30. The contraction of the connective tissue causes widening of the vessels in the new-formed tissue; and there may be produced, as in Fig. 30, a tissue with large channels, and through these the circulation and the function of the vein may be restored. A favourite place for the formation of this cavernous tissue is the place of union of the iliac veins to form the vena cava. Here the vessels are sometimes found filled with a spongy tissue through which the circulation is carried on. By a still further contraction of the new-formed tissue, the calibre of the vessel may be completely re-established, the sinus-like blood-channels expanding into the calibre of the vessel.

Fig. 80. - Vein of leg filled with thrombus, which has become completely organized. New-formed vessels are shown, which have widened greatly so as to partially restore the circulation, x'25.
In studying thrombosis, we have left out of account all cases of what is called septic thrombosis, where the coagulation arises in connection with the introduction of decomposing material into the veins. Such processes will receive consideration in another part.
Embolism is a frequent consequence of thrombosis in any situation. (See under Embolism).
Thrombosis in veins leads most directly to passive hyperemia with its consequent oedema and dropsy, and sometimes haemorrhage. The occurrence of serious oedema depends largely on the extent of the anastomosis of the obstructed veins, and also somewhat on the rapidity with which the thrombosis has occurred. If the thrombus forms slowly the functions of the plugged veins may be largely taken up by the lymphatics and by other veins which remain unaffected. In the case already referred to, where a cancerous tumour in the kidney had burst into the renal vein, and thrombosis had extended to the vena cava and down the veins of both legs, there was comparatively little oedema at any time, although all the main venous trunks of both legs were plugged. The fact that the thrombosis does not extend into the capillaries allows the circulation to be carried on by arteries, capillaries, and lymphatics.
At the seat of thrombosis there is usually an inflammation, which may be of considerable intensity, and is sometimes accompanied by considerable pain. Even when the thrombus does not include specially irritating material, there is inflammation of the wall, leading, especially in the case of veins, to adhesion to parts around, with induration (Periphlebitis). A periphlebitis, accompanied by considerable oedema and by severe pain, occurs in Phlegmasia alba dolens.
It is important to know that these secondary effects of thrombosis, and especially oedema, will not usually show themselves for some time after the onset of the process. A coagulation beginning in a vein will take some time before it completely obstructs it, and even when it has done so, it may be necessary for it to grow into other veins before any pronounced oedema will develop. Hence it is that a thrombosis may lead to embolism by detachment of portions of the thrombi before it has manifested its presence by hypersemia and oedema.
Thrombosis in veins seldom leads to Gangrene, and in the few cases in which gangrene actually occurs some additional interference with the circulation will usually be discoverable. Weakening of the heart, in conjunction with thrombosis, may cause it, and so may disease of the arteries diminishing the force of the blood.
Thrombosis in arteries, occurring, as it does, chiefly along with atheroma, may have as its result ischemia and its consequences. (See above).
Buchanan, Proceedings of Phil. Sou. of Glasg., 1845; Schmidt, various papers and Die Lehre v. d. fermentativen Gerinnungserscheinungen, 1876; Rauschenbach, Protoplasma und Blutplasma, 1882; Foa and Pellacani, Arch, ital. de Biologie, iv.; Hayem, Arch, de physiol., 1878, 1879; Bizzozero, Virchow's Archiv, vol. xc, 1882; Wooldbidge, Chemistry of the blood, etc., 1893; Lowit, Arch. f. exper Path., vol. xxiv., 1887; Virch. Arch., vol. cxvii., 1889; Studien zur Phys. u. Path, des Blutes, 1892; Eberth und Schimmelbusch, various papers in Virchow's Archiv, vols, ci., ciii., cv., cviii.; Zahn, Virchow's Archiv, vol. lxii.; Virchow, Ges. Abhandlungen, 1856, and Handbuch der spec. Path. u. Therap., vol. i.; Baumgarten, Die Organization des Thrombus, 1877; Recklinghausen, Handbuch, p. 133; Wright, Journ. of Path., i., 1893; Freund (with complete literature) in von Limbeck's Path, des Blutes, 1896.
 
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