Homogenization of thrombus After 1 d of thrombus formation, its surface is covered by endothelium as a new fresh red thrombus. After a certain period of time, the red blood cells and white blood cells inside the thrombus disintegrate, and both white and red thrombi become homogenized, and after a long time the thrombus becomes gray and homogeneous. At the same time, the size of the thrombus is reduced due to drying and shrinkage. Softening and dissolution of thrombus The natural law of thrombus formation is basically the autolysis process. The solid protein material contained in the thrombus is dissolved by the action of enzymes. When a thrombus dissolves, it starts from the inside and forms a cavity in the center. Smaller thrombi can dissolve completely and disappear, while larger thrombi soften only internally and mechanize on the surface. Mechanization of thrombus recanalization The mechanization process of thrombus begins on the second to third day of thrombus formation. From about the fourth day, the thrombus can adhere to the vessel wall because it is invaded by the new blood vessels and connective tissues in the endothelium. Eventually the connective tissue matures and contracts, and this part of the thrombus shrinks. When thrombus mechanization begins, granulation tissue with myofibroblasts and histiocytes rich in capillaries enters the thrombus and engulfs and lyses it, allowing recanalization of the thrombus-obstructed vessel. However, blood flow is usually too low to effectively restore blood flow, and the thrombotic remnants still have a mesh-like fibrin present that can form extensive vortices, making the thrombus vulnerable to reoccurrence. The consequences of thrombosis depend on the cause, location, speed, extent, and compensatory side branch establishment of thrombus formation. Venous thrombosis is usually more common in the lower extremity and is often partially compensated and less likely to be necrotic because of the greater number of venous anastomotic branches and the ease of establishing collateral circulation. Only in the case of sudden complete iliac-femoral vein thrombosis in the lower extremity, acute reflux obstruction occurs in the deep vein, and the limb is extremely swollen, causing arterial spasm or occlusion, lower extremity ischemia and tissue necrosis, which is clinically called “femoral cyanosis”, and if not treated in time, there is a risk of limb necrosis and amputation; venous thrombosis can be dislodged and often cause pulmonary artery Embolism can be caused by dislodged venous thrombus, and large pieces can cause fatal pulmonary infarction. The microthrombus formed by DIC can cause microcirculatory disorders in the heart, brain, lungs, kidneys and other important organs, and even multi-system organ failure, which is life-threatening. It should be noted that a significant portion of the “thrombus recanalization” seen in clinical practice is not really recanalization, but circulatory rebuilding, mainly related to the establishment of side branch compensation. For example, deep vein thrombosis in the lower extremities, early dilatation of superficial veins in the femur and lower legs is often seen. Dilation of vessels, elimination of hypercoagulable state, improvement of hemodynamics and dissolution of thrombus form non-surgical conservative treatment methods. In the later stage, the superficial veins have dilated and gradually become varicose, and the swelling of the limb is better compared with the acute stage, but the limb is still swollen, pigmentation, dermatitis and chronic ulcers occur, which is called the sequelae of deep vein thrombosis in the lower limbs. The thrombus has been mechanized, connective tissue invasion and contraction to recanalization, and the mesh-like fibrin remains in the venous cavity, which affects the smooth blood return, and the conservative drug treatment only prevents thrombus re-formation, and must be combined with surgical treatment to unblock and reconstruct the circulation.