The three basic factors of thrombosis are slow blood flow and vortex formation, increased coagulation and intimal injury, which are also the main causes of this disease.

(2) Pathogenesis

Thrombosis can occur in both vein and arterial lumen, the former is mainly due to increased coagulation, and the latter is based on intimal injury.

1. Slow blood flow and vortex formation are important conditions for thrombosis. Such as long-term bed rest, heart failure, tumor compression, varicose veins and venous tumors, increased abdominal and pelvic pressure during pregnancy, and muscle contraction weakness of lower limbs, can all cause slow blood flow and promote thrombosis. The reason is that the slow blood flow widens the axial flow, which is beneficial to the lateral and agglutination of platelets and increases the chance of contact and agglutination with intima; At the same time, local agglutinating platelets and a small amount of blood coagulation active substances can not be diluted and removed because of slow blood flow, and they gather locally to reach the necessary concentration for coagulation; Coupled with slow blood flow, vascular endothelial cells are vulnerable to injury, collagen exposure and thrombosis. In addition, after the formation of varicose veins and venous tumors, the local blood flow state changes, resulting in vortex, which makes platelets precipitate, precipitate and coagulate from the blood flow, and is also easy to cause thrombosis.

2. Blood coagulation increases, platelets or coagulation factors increase, fibrinolytic activity decreases, and blood coagulation increases to cause thrombosis. Water loss and blood loss caused by various reasons lead to blood concentration; The number and viscosity of platelets increased; The content of coagulation factors such as fibrinogen and prothrombin increased; Advanced cancer, such as pancreatic cancer and lung malignant tumor, can activate exogenous coagulation system due to the release of thromboplastin-like substances from tumor necrosis; Some allergic diseases may cause the destruction of platelets and red blood cells, release platelet factor 3 and red blood cell toxin, and activate prothrombin, which are beneficial to thrombosis.

3. Various causes of intimal injury, such as trauma (intravenous sclerosing agent, hypertonic solution, anticancer drugs, contrast agent, intravenous intubation), hypoxia, chemicals (smoking, hypercholesterolemia), infection (bacterial toxin), tumor cell invasion, etc. It can cause vascular endothelial cell damage, lead to rough exposure of subcutaneous collagen fibers and promote platelet aggregation. ADP and thromboxane A2 are released from aggregated platelets and endothelial cells, further promoting platelet aggregation. At the same time, the exposed collagen fibers activate the first factor in blood, and then start the endogenous coagulation system, and the tissue coagulation factor released from the damaged intima starts the exogenous coagulation system, thus causing blood coagulation and promoting thrombosis.

Venous thrombosis can occur in all parts of the body. The most common is the great saphenous vein and its branches, and the rare ones are popliteal vein, subclavian vein, cephalic vein, basilic vein and thoracoabdominal vein. After superficial venous thrombosis of lower limbs or upper limbs, tissue edema is not easy to occur because of the wide anastomotic branches. On the contrary, large deep veins, such as iliofemoral vein, axillary vein, superior vena cava and inferior vena cava, hinder blood return due to lumen stenosis or occlusion after thrombosis, and the venous pressure increases due to the outward development of thrombus, resulting in congestion of capillaries and venules, tissue hypoxia, and then the osmotic pressure of capillaries increases, resulting in tissue edema. When lymphatic vessels are compressed, edema is more obvious. In the future, if new blood vessels are formed or recanalized and collateral circulation is established, the blood circulation of the affected area will be maintained. If these newly formed structures are sound, venous reflux will also be improved (but it is difficult to recover when venous valves are damaged). On the contrary, it will lead to chronic venous insufficiency, post-phlebitis syndrome or partial thrombosis falling off and becoming embolus.

Venous thrombosis and

thrombophlebitis

The difference is that the former is mainly slow blood flow and increased coagulation, while the venous wall changes little; The latter is thrombosis on the basis of existing inflammation of vein wall. Thrombosis was found in the venous cavity during pathological anatomy, but there was no obvious clinical manifestation of thrombophlebitis before death. On the contrary, within a few hours after thrombosis, we can see that the blood vessel wall has different degrees of inflammatory reaction. So it is difficult to distinguish clearly in clinic, so it can be collectively called thrombophlebitis.

Fresh thrombi in great veins are usually mixed. Typical thrombus is divided into three parts: head, body and tail. On the intima of diseased vein, gray thrombus was formed with adhered platelets and mixed leukocytes as the head. On the basis of white thrombus, more white blood cells, fibrin and a large number of red blood cells are attached to form mixed thrombus as the body; When the formed thrombus develops further and fills the lumen, the local blood flow stops, and the blood coagulates rapidly, forming a dark red thrombus as the tail. The length of a thrombus usually ends in an effective vascular branch. Thrombosis is dissolved by fibrinolytic enzyme and neutrophil proteolytic enzyme. Within 5 days after thrombosis, fibroblasts invaded and formed new granulation tissue, which was then organized to form and recanalize new blood vessels. If connective tissue hyperplasia and scar formation, the diseased vein will become sclerosing spinal cord injury.

The histopathology of thrombophlebitis caused by different reasons is not completely the same, such as purulent phlebitis, whose wall inflammation is obvious, mainly neutrophil infiltration; Chemical phlebitis has obvious intimal hyperplasia; In phlebitis caused by tumor and heart failure, the inflammatory reaction of the tube wall is relatively light; Fibroblast reaction in the wall and surrounding tissues of wandering thrombophlebitis is serious.