(A) Etiology
The classical Virchow theory suggests that damage to the vessel wall, abnormal blood flow and altered blood composition are the 3 main factors causing venous thrombosis. The alteration of blood composition into hypercoagulable state is the determinant of DVT formation.
15 susceptibility factors.
1, age: age increases, the incidence rate gradually increases, the incidence rate of 80-year-old people is more than 30 times that of 30-year-old people.
2, braking: clinically it is often seen that patients who are bedridden for a long time are prone to DVT, and venous blood return is significantly slowed down after braking, which increases the risk of DVT development.
3, history of venous thrombosis 23% to 26% of patients with acute DVT have a previous history of venous thrombosis, and these newly formed thrombi are often from the original lesion of the vein. It was found that the blood of recurrent DVT patients is often in a hypercoagulable state.
4, malignant tumor statistics found that 19% to 30% of DVT patients combined with malignant tumors, lung cancer is the most likely to cause DVT a malignant tumor, other malignant tumors such as genitourinary system and gastrointestinal system is also prone to complicate DVT.
5, surgery: surgery is an important susceptibility factor of DVT, in which the type of surgery is particularly important. The incidence of DVT after general surgery is around 19%, neurosurgery is around 24%, while femur fracture, hip arthroplasty and knee arthroplasty are as high as 48%, 51% and 61% respectively.
6, trauma: autopsy of traumatic death found that 62% to 65% of the deceased had DVT occurrence.
7.Primary blood hypercoagulability: common in patients with genetic mutations or hereditary anticoagulant defects, 5%-10% of all DVT patients are caused by primary blood hypercoagulation.
8, postpartum: the incidence of postpartum DVT is higher, while DVT patients in domestic pregnancy is less common.
9, oral contraceptives: oral contraceptives are prone to DVT, it has been found that 1/4 of women of childbearing age suffering from DVT are related to taking contraceptives, and 8 times more women of childbearing age taking third-generation contraceptives have DVT complications than those not using contraceptives.
10, blood type: blood type and DVT have been found to have a certain relationship, people with A blood type are most likely to suffer from DVT, relatively speaking, O blood type has the least risk of DVT.
11.Ethnicity: The incidence of DVT is much higher in Europe than in Asia, and the difference of living habits and dietary structure may also affect the occurrence of DVT.
12.Central venous cannula: clinically, central venous cannula is increasing, which makes the incidence of DVT also increase accordingly, especially in the upper extremity DVT, 65% of the patients are related to central venous cannula.
13.Enteritis: Pulmonary embolism in patients with enteritis is often reported clinically.
14.Systemic lupus erythematosus patients are often combined with arteriovenous thrombosis.
15.Other: whether obesity, varicose veins of lower extremities and cardiac insufficiency are susceptibility factors of DVT is still debated, and multi-factor statistical analysis suggests that obesity, varicose veins of lower extremities and cardiac insufficiency are not independent susceptibility factors.
(B) Pathogenesis
1.Pathology
There are three types of venous thrombosis: white thrombosis, red thrombosis and mixed thrombosis. White thrombosis is mainly composed of fibrin, platelets and white blood cells, and contains only a small amount of red blood cells. Red thrombus is mainly composed of a large number of red blood cells, fibrin, and contains a small amount of platelets and white blood cells. White thrombus and red thrombus are often mixed together to form a mixed thrombus. When a venous thrombus is first formed, it is a white thrombus, which forms the head of the thrombus, while its secondary derivatives, the body and tail, are mainly red thrombi.
Once formed, venous thrombosis is in a continuous process of evolution. On the one hand, as venous thrombosis narrowed or occluded the venous lumen, new thrombi were formed on the surface of venous thrombus, which were derived to the proximal and distal ends, respectively, and there was no adhesion between the proximal thrombus and the venous wall in the early stage, and the thrombus floated in the lumen and was easily dislodged, resulting in pulmonary embolism, and later fibroblasts and budding capillaries invaded the thrombus, and the thrombus formed close adhesion with the wall after mechanization. On the other hand, in the early stage of venous thrombosis, endothelial cells on the surface of the affected vein secrete thrombolytic substances and dissolve the thrombus. At the same time, leukocytes, especially monocytes, invade the thrombus and activate urokinase-type fibrinogen activator (u-PA) and tissue-type fibrinogen activator (t-PA) to enhance the thrombolytic activity, resulting in the formation of many fissures within the venous thrombus. The thrombolytic effect and the contraction and fragmentation of fibers within the thrombus cause the fissures to expand, and new endothelial cells gradually migrate and grow on the surface of the fissures, eventually recanalizing most of the blocked veins. The valves of these recanalized veins are often disrupted and a portion of the lumen is left with fibrous adhesions. The length of the venous recanalization process varies and generally takes six months to 10 years.
Lower extremity iliofemoral vein thrombosis is more common on the left side, two to three times as often as on the right side, probably because the left iliac vein has a longer path and the right iliac artery crosses over it, causing the left iliac vein to be compressed to varying degrees.
After lower limb venous thrombosis, especially trunk vein thrombosis, blood return to the affected limb is blocked. In the acute phase, blood cannot return through the trunk vein, causing a rapid increase in intravenous pressure, and water in the blood seeps into the tissues through capillaries, resulting in tissue swelling. At the same time, the increased venous pressure forces the lateral branch veins to dilate and open, and the stagnant blood returns through the lateral branch veins, causing the swelling to gradually subside.
2.Pathological classification
(1) According to the embolism vascular site: there are 3 types of DVT in lower limbs, namely peripheral type, central type and mixed type.
(1) Peripheral type: also known as calf muscle plexus thrombosis, after thrombosis, most of the symptoms are mild because the thrombus is limited. After treatment, most of them can be ablated or mechanized, or can be autolyzed. A small number of untreated or improperly treated emboli can expand into the thigh and become mixed. Dislodgement of small emboli can cause mild pulmonary embolism, which is often clinically overlooked.
The main clinical manifestations are pain and mild swelling in the lower leg and limitation of movement. The symptoms are consistent with the time of thrombosis. The main signs are pain caused by pulling the gastrocnemius muscle during foot dorsiflexion (positive Homan’s sign) and gastrocnemius pressure pain (positive Neuhof’s sign).
②Central type: also known as iliofemoral vein thrombosis. It is more common on the left side and presents with swelling below the buttocks, anger in the lower extremities, groin and superficial veins of the affected abdominal wall, elevated skin temperature and pressure pain towards the deep veins. The thrombus may extend upward to the inferior vena cava and downward to involve the entire lower extremity deep veins in a mixed pattern. Thrombus dislodgement can lead to pulmonary artery embolism and threaten the patient’s life.
(3) Mixed type: In other words, thrombus is formed in the deep veins of the whole lower extremity and the muscular venous plexus. It can be extended from peripheral type, and the symptoms are not noticed at the beginning, but the swelling level rises gradually until the edema of the whole lower limb is detected. Therefore, the clinical presentation is not consistent with the time of thrombosis. It can also be caused by the downward expansion of the central type, and its clinical manifestations are not easily distinguished from those of the central type.
(2) According to the scope of involvement: According to the scope of vessels involved in embolism, lower limb deep vein embolism is divided into whole limb type and focal segment type.
(1) Whole limb type: The lesion involves the whole lower limb deep vein trunk. According to the degree of recanalization, there are 3 types: type I, complete occlusion of the deep venous trunk; type II, partial recanalization of the deep venous trunk, of which there are 2 subtypes. Type IIA, partial recanalization is mainly occlusion, and only segmental recanalization is shown; Type IIB, partial recanalization is mainly recanalization, the deep vein has been continuous channel, but the diameter of the tube is uneven, and recanalization is incomplete. The hemodynamics of type I and II are dominated by impaired deep venous blood return. In type Ⅲ, the deep venous trunk is completely recanalized, but the valves are all destroyed, the wall is stiff, or dilated and tortuous, and its hemodynamics has changed from obstructed reflux to backflow.
②Focal segment type: the lesion is limited to part of the venous trunk, such as iliac vein, iliac-femoral vein, superficial femoral vein, femoral-N vein, N vein, tibiofemoral trunk vein, gastrocnemius plexus, or calf deep vein thrombosis sequelae.