I. Overview
In the lumen of the heart or blood vessels of a living body, the process by which blood coagulates or some of the organic components of blood adhere to each other and form a solid mass is called thrombosis, and the solid mass formed in this process is called a thrombus. This article mainly deals with venous thrombosis.
Second, the causes of thrombosis
1.Stagnant venous blood flow During surgery, spinal anesthesia or general anesthesia leads to dilatation of peripheral veins, slowing down of venous flow, complete paralysis of lower limb muscles, loss of contraction function, and bed rest after surgery due to incision pain and other reasons, resulting in relaxation of lower limb muscles, which leads to stagnant blood flow and induces deep vein thrombosis of lower limb.
2.Venous wall injury Various factors damage the venous blood vessel wall, leading to or complicating venous thrombosis, commonly mechanical injury venous local contusions, lacerations or fracture fragment trauma.
3, blood hypercoagulation state is one of the basic factors causing venous thrombosis. Various large-scale surgery is to cause hypercoagulable state, platelet adhesion ability is enhanced; after splenectomy due to the sudden increase of platelet, can increase blood coagulation, burns or serious dehydration to make blood concentrated, also can increase blood coagulation. Advanced cancer, such as lung cancer and pancreatic cancer, often releases many substances when cancer cells destroy tissues at the same time, thus increasing blood coagulation. High dose application of hemostatic drugs can also make the blood in a hypercoagulable state.
The two main causes of venous thrombosis are stagnant venous blood flow and hypercoagulable blood. A single factor cannot yet cause the disease independently, but often the combination of two or three factors causes deep vein thrombosis. For example, the high incidence of postpartum deep vein thrombosis is due to a combination of factors.
Third, the regression after thrombosis
1.In the acute phase of venous thrombosis, when the venous blood return of the lower limb is obstructed, the high pressure venous blood on the distal side of the thrombus will increase the return flow by using all the traffic branches which usually do not play an important role, and if the effective side branch circulation is not established, it will cause local bruising, edema, pain, bleeding, and even necrosis.
2.The spread of thrombus can follow the direction of venous blood flow and extend to the proximal end. When the thrombus completely obstructs the main trunk of the vein, it can extend retrogradely.
3.Embolism, before the thrombus is firmly adhered to the vessel wall, the whole or part of the thrombus can be dislodged and form an embolus, which runs with the blood flow and causes embolism. Lower extremity deep vein thrombosis can cause pulmonary embolism with symptoms such as chest tightness and breathlessness, and thrombus obstruction of pulmonary artery trunk can endanger the patient’s life in a short time.
4, thrombus can be mechanized, re-tubularization and re-endothelialization, so that the venous lumen to restore a certain degree of patency. However, the effect of the contraction of the lumen love fibrous tissue and the destruction of the venous valve itself can lead to secondary deep venous valve insufficiency and produce post-venous thrombosis syndrome.
IV. Clinical manifestations
1, symptoms: the most common main clinical manifestation is the sudden swelling of one side of the limb, local pain, and intensify when walking. In mild cases, the local sensation is only heavy, and the symptoms are aggravated when standing.
2. Signs: Physical examination has the following features: swelling of the affected limb. When the swelling of the lower leg is severe, it often leads to increased tissue tension; pressure pain. There is often pressure pain at the site of venous thrombosis.
V. Auxiliary examination
1.Ultrasonic examination: two-dimensional ultrasound imaging can directly see the thrombus in the large vein, together with the measurement of blood flow velocity in the vein. The diagnostic sensitivity of this kind of examination for proximal deep vein thrombosis is up to 95%; for distal ones, the diagnostic sensitivity is only 50%-70%, and for abdominal external iliac vein and common iliac vein thrombosis, the accuracy is reduced because of the interference of abdominal organs.
2.Plasma D-dimer measurement: D-dimer is a specific marker of fibrinolytic process, and increased or positive is seen in secondary fibrinolytic hyperfunction. There are many influencing factors, including myocardial infarction, cerebral infarction, pulmonary embolism, venous thrombosis, surgery, tumor, diffuse intravascular coagulation, infection and tissue necrosis, etc., which can lead to elevated D-dimer, so the results must be verified.
3.Impedance volume tracing method and venous flow tracing method: the positive rate of this test for the diagnosis of proximal deep vein thrombosis can reach 90%, but the sensitivity of the diagnosis for the distal end is obviously reduced.
4.Radionuclide examination: Iodine 125 fibrinogen scan is occasionally used for the diagnosis of this disease. In contrast to ultrasonography, the detection rate of deep vein thrombosis in the interior of the gastrocnemius muscle can be as high as 90%, while the specificity for the diagnosis of proximal deep vein thrombosis is poor. The main disadvantage of this test is that it requires a lag of 48-72 hours after injection of radionuclide before the results can be displayed.
5.Superior venography: the patient lies on his back, 40-50ml of contrast agent is injected from the superficial vein of the foot within a short time, and a pressure band is used at the proximal end, which can easily make the contrast agent enter into the deep venous system directly, and if there is a venous filling defect, qualitative and local diagnosis can be made. This test is the gold standard for the diagnosis of this disease and the basis for determining the next interventional route for thrombolytic therapy, as it allows observation of the entire length of the external/common iliac vein from the lower leg to the lower abdomen, and the location and extent of the thrombus. It can also observe the condition of the venous valves.
Sixth, clinical stage
1.Acute stage: within 14 days after the onset of the disease.
2.Sub-acute stage: between 15 and 28 days after onset.
3.Chronic phase: after 28 days of onset.
4. post-acute phase: symptoms of venous insufficiency (post-thrombotic syndrome).
5.Acute attack in the chronic or post-acute phase: another acute attack of the disease in the chronic or post-acute phase.
VII. Diagnosis
1.Most often seen in postpartum, post-pelvic surgery, trauma, advanced cancer, coma or patients who are bedridden for a long time.
2.The onset of the disease is acute, the affected limb is swollen and hard and painful, which is aggravated after activity, often accompanied by fever and rapid pulse.
3.The thrombus site is painful, and cords can be found along the blood vessels. The limb distal to the thrombus or the whole limb is swollen, and the skin is blue-purple, or venous gangrene appears. When the thrombus extends to the inferior vena cava, the two lower limbs, buttocks, lower abdomen and external genitalia are obviously edematous.
4.Late thrombus absorption and mechanization often leave venous insufficiency, birth superficial varicose veins, pigmentation, ulceration, swelling, etc., which is called deep vein thrombosis post-formation syndrome.
5.Thrombus dislodgement may lead to pulmonary embolism.
Eight, treatment measures
1.Interventional treatment
Inferior vena cava filter placement: The thrombus may form large and small blocks after thrombolytic drug application and dislodge, forming a tether, which returns with blood flow toward the heart and then enters the pulmonary artery. A small embolus can cause the symptoms of pulmonary embolism such as chest pain, chest tightness and breathlessness in a short period of time, while a large tether will endanger the patient’s life if it blocks the main trunk of the pulmonary artery (usually the patient dies within 10-30 minutes due to “suffocation”). Therefore, a filter should be placed in the inferior vena cava (the proximal end of the thrombus) before thrombolytic therapy to prevent large emboli from entering the pulmonary artery.
Thrombolytic therapy with cannulae After the formation of thrombus, the deep veins of the lower limbs are completely filled with thrombus, and the blood flow cannot pass through them. Interventional treatment is to insert a catheter into the lower extremity deep vein thrombus through puncture at a suitable site, and “open” a small channel inside the thrombus first to allow venous blood flow to pass through the thrombus, and then inject thrombolytic drugs into the thrombus under pressure through the catheter to promote thrombus dissolution.
The key to interventional treatment of lower extremity deep vein thrombosis is the successful placement of the catheter in the thrombus, and the appropriate puncture access is an important guarantee of successful placement. At present, the main puncture routes are: through the jugular vein, through the contralateral femoral vein, through the superior femoral vein of the affected side, through the superior N vein of the affected side, through the inferior femoral vein of the affected side, etc. Among them, the superior N vein is more in line with the biological characteristics of the disease, and is the first choice for the current catheterization scheme.
2.Non-surgical treatment
Interventional placement of thrombolysis should be accompanied by corresponding non-surgical treatment
3.Surgical treatment
That is, surgical thrombus removal, because the thrombus can still be formed again after surgery, it is rarely used now.
In recent years, for patients in the chronic stage within 6 months after thrombosis, there are reports of cases of complete ablation of thrombus through interventional treatment, therefore, for patients 1-6 months after thrombosis, active interventional treatment is also recommended.
IX. Complications
If lower extremity deep vein thrombosis is not treated in time, the long-term existence of thrombus will cause a series of complications
Pulmonary embolism.
In the early stage of lower extremity deep vein thrombosis, the thrombus is relatively fragile and easy to dislodge within a few days, especially the thrombus dislodged from the iliac-femoral vein, which is large enough to block the main trunk of pulmonary artery and its branches, with significant clinical manifestations, easily leading to respiratory and circulatory failure and even sudden death. Fatal pulmonary embolism.
Superficial varicose veins of the lower extremities.
After the occurrence of deep vein thrombosis in the lower extremity, blood cannot return due to venous obstruction, and the venous system of the extremity is severely stagnant, blood return must be through secondary venous vessels, and the superficial veins of the lower extremity appear dilated or varicose, and can make the fine veins fill and expand, superficial varicose is the compensatory reaction of the body secondary to the formation of deep vein thrombosis, and the varicose veins can be combined with infection due to slow blood flow and lead to thrombotic superficial phlebitis.
Lower extremity deep vein valve insufficiency.
In the process of thrombosis and recanalization, the deep vein valve is damaged and loses its normal function, resulting in blood backflow. The symptoms of lower limb deep vein valve insufficiency include weakness, soreness and swelling of the lower limbs, and there may be calf muscle twitching, and the symptoms are aggravated in the afternoon and when walking, and are lighter in the morning, and can be relieved by elevating the affected limbs.
Skin pigmentation in the foot and boot area.
Stasis dermatitis is due to long-term high pressure stasis in the venous system of the lower extremities, long-term compensatory expansion of superficial veins and other causes loss of venous valve function, further aggravating the stasis, extensive interstitial fibrosis, dense and hardened skin and subcutaneous tissue, increased capillary pressure and long-term stasis can occur bleeding and pigmentation of the lower leg.
Chronic stasis ulcers.
Because the lower extremity is in a state of venous hypertension stasis, some tissues appear interstitial edema, compression of capillaries and small arteries reduces blood supply to skin and subcutaneous tissues, accompanied by venous stasis with reduced oxygen content and accumulation of metabolites, local tissue circulation and metabolic disorders, thin skin and subcutaneous tissues, skin rupture, formation of ulcers mostly located in the inner part of the ankle, easy to secondary staphylococcal or streptococcal infection with pain, The skin and subcutaneous tissues are thin and the ulcers are mostly located on the medial side of the ankle.
Inferior vena cava occlusion syndrome.
The clinical manifestations of this syndrome are mainly the symptoms caused by the obstruction of deep venous return in both lower limbs, such as swelling, heaviness, varicose or dilated superficial veins, and dilated superficial genital veins, because the blockage plane is mostly located on the distal side of the renal vein plane. If the lesion involves renal vein or above planes, renal dysfunction and manifest back pain, kidney enlargement, and in serious cases, proteinuria and hematuria, and if the lesion involves hepatic vein or above planes, there may be manifestation of Buga’s syndrome, and the prognosis is poor.
Lymphedema.
Long-term venous insufficiency and stasis, swelling often leads to lymphovascular inflammation, venous edema and lymphedema coexist.