Deep vein thrombosis of lower extremities
Deep vein thrombosis of the lower extremities is most common in the iliofemoral section of the lower extremities. This disease can be followed by lower extremity edema, secondary varicose veins, dermatitis, hyperpigmentation, and depressed ulcers, which seriously damage the health of working people.
[Etiology].
There are three major factors of venous thrombosis: stagnant venous blood flow, venous wall damage and blood hypercoagulation. They are described as follows.
(a) Stagnant venous blood flow: spinal anesthesia or general anesthesia during surgery leads to dilatation of peripheral veins and slows down the venous flow; the muscles of the lower limbs are completely paralyzed and lose their contraction function due to anesthesia during surgery, and the muscles of the lower limbs are still in a relaxed state when resting in bed after surgery, resulting in stagnant blood flow and triggering the formation of deep vein thrombosis in the lower limbs. It is reported that the longer the operation lasts, the more likely deep vein thrombosis will occur, and most of the thrombosis starts in the peripheral veins of the lower leg.
(B) The injury of vein wall
1. Chemical injury: venipuncture or injection may damage the vein lining to varying degrees, leading to phlebitis and venous thrombosis.
2. Mechanical injury: local contusions, lacerations or fracture fragment trauma to veins can produce venous thrombosis.
3. Infectious injury: septic thrombophlebitis is caused by perivenous infection foci, which is less common.
(C) blood hypercoagulable state: this is one of the basic factors that cause venous thrombosis. Various large surgeries, burns, advanced cancer or severe dehydration can increase blood coagulation; long-term use of contraceptives or high-dose application of hemostatic drugs can also increase blood coagulation.
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.
Pathological changes]
Venous thrombosis can be divided into three types: ① red thrombus or coagulation thrombus, which is relatively uniform in composition, with platelets and leukocytes scattered within a gelatinous mass of red blood cells and fibrin; ② white thrombus, which includes fibrin, layered platelets and leukocytes, and only a very small number of red blood cells; ③ mixed thrombus, which is the most common and contains white thrombus forming the head, lamellar red thrombus and white thrombus forming the body, and red thrombus or lamellar thrombus constitutes the tail.
Deep vein thrombosis in the lower extremities originates in some cases in the calf veins and in others in the femoral and iliac veins.
The pathophysiological changes caused by venous thrombosis are mainly due to the various effects of venous return disorders. The degree of venous blood return obstruction depends on the size and location of the involved vessels, as well as the extent and nature of thrombosis. After the formation of venous thrombosis, a series of pathophysiological changes caused by the increase of venous pressure on the distal side of the thrombus, such as the small veins and even capillary veins are in an obvious depressed state, the osmotic pressure of capillaries increases due to the change of venous pressure, and the permeability increases due to the lack of oxygen in the endothelial cells of blood vessels, so that the intravascular fluid components leak outward and move to the tissue interstices, often resulting in swelling of the limbs. If there is leakage of red blood cells outside the blood vessels, their metabolites contain iron-containing heme, forming skin pigmentation.
In the case of venous thrombosis, it can be accompanied by a certain degree of arterial spasm, which, in the case of weakened arterial pulsation, causes lymphatic depression and impaired lymphatic return, aggravating the swelling of the limb.
In addition, during the process of venous thrombosis, the inflammatory reaction of the vein itself and its surrounding tissues, the rapid increase of venous pressure on the distal side of the thrombus, the sudden expansion of the vein, the edema of the lower limb caused by the obstruction of lymphatic return, and the arterial spasm caused by venous thrombosis, which puts the limb in a state of hypoxia, all these series of pathophysiological changes can cause painful symptoms of varying degrees.
In the acute phase of venous thrombosis, when blood return to the main veins of the limb is impaired, high-pressure venous blood distal to the thrombus will increase return using all the traffic branches that are not normally important. For example, superficial venous anastomotic branches in the upper thigh and lower abdomen may pass to the contralateral trunk and upward through the abdominal wall to the odd vein and the intrathoracic venous system. In the deeper part, anastomotic branches may reach the contralateral internal iliac vein through the pelvic venous plexus. Adaptive dilatation of these veins promotes cardiac return of venous blood distal to the thrombus.
The spread of the thrombus may follow the direction of venous flow and extend proximally, as in the calf where the thrombus may continue to extend into the inferior vena cava. When the thrombus completely obstructs the venous trunk, it can extend retrogradely. Fragments of the thrombus can also be dislodged and follow the blood flow through the right heart and then embolize in the pulmonary artery, which is a complication of pulmonary embolism.
On the other hand, the thrombus can be mechanized, re-tubularized and re-endothelialized to restore some degree of patency to the venous lumen. The process of thrombus mechanization starts from the periphery and proceeds gradually to the center. The degree of progression varies. Degenerative changes in the thrombus may occur as a result of the action of fibrinolytic enzymes in the blood, or as a result of cellular autolysis and phagocytosis. Another important process of mechanization, the growth of endothelial cells and their penetration into the thrombus, is an important component of retubulation. In clinical observations, it has been found that re-tubularization is a long course of disease, taking about 8-15 years. The final result of the organism will restore some degree of function to the veins. However, the lumen is affected by the contraction of fibrous tissue and the venous valve itself suffers damage, so that the valve disappears or adheres to the wall in a hypertrophic manner, which leads to secondary deep venous valve insufficiency and produces post-venous thrombosis syndrome.
Clinical manifestations]
The most common main clinical manifestation is the sudden swelling of one limb, local pain, which is aggravated when walking. In mild cases, the local heaviness is only felt, and the symptoms are aggravated when standing. Physical examination has the following features: ① Swelling of the affected limb. The degree of development of swelling is reliable only if it is accurately measured daily with a tape measure and compared with the thickness of the healthy lower limb, which is not reliable by visual observation alone. This sign is of high value to confirm the diagnosis of deep vein thrombosis, and when the swelling of the lower leg is severe, it often leads to increased tissue tension; ② pressure pain. There is often pressure pain at the site of venous thrombosis. Therefore, the lower limbs should be examined for calf muscles, N fossa, adductor canal and femoral vein below the groin; ③Homans sign. When the foot is sharply bent to the dorsal side, it can cause pain in the deep calf muscle. Homans’ sign is often positive in the case of deep calf vein thrombosis. This is caused by the passive elongation of gastrocnemius and flounder muscles, which stimulates the whole vein of calf blood; ④ superficial varicose vein. Deep vein obstruction can cause elevated superficial venous pressure and cause secondary superficial venous dilatation.
According to the different parts of venous thrombosis, different clinical manifestations can appear, which are described as follows.
1. Calf deep vein thrombosis: Although the calf deep vein is the most likely site of postoperative thrombosis, it is sometimes underdiagnosed. Common symptoms include pain and pressure in the calf, mild swelling or insignificant swelling in the calf, positive Homans sign, and normal superficial venous pressure.
2. Femoral vein thrombosis: Most of the femoral vein thrombosis is secondary to deep vein thrombosis in the lower leg. However, a few femoral vein thrombosis can exist alone. The signs are pressure pain at the site of the adductor canal, the N fossa and the deep calf. Homans’ sign is positive or negative.
3. Iliofemoral vein thrombosis: Most of the iliofemoral vein thrombosis is secondary to deep vein thrombosis in the lower leg, but sometimes it is primary in the iliofemoral vein or iliac vein. Postpartum women, pelvic fractures, pelvic surgery and patients with advanced cancer are prone to it. The lesions occur 2 to 3 times more often in the deep veins of the left lower extremity than in the right. This may be due to the longer course of the left common iliac vein and the compression of part of the left common iliac cavity by the right common iliac artery. Occasionally, it may also be due to a congenital reticular malformation at the junction of the left common iliac vein with the inferior vena cava.
The onset of the disease is rapid, with pain, tenderness, and marked swelling of the entire affected limb within hours. The superficial veins of the upper femur and the ipsilateral lower abdominal wall are dilated. There is significant tenderness along the femoral triangle and in the area of the femoral adductor canal. The femoral vein may be palpable and painful in the area of cords. In severe cases, the skin color of the affected limb is cyanotic, called “femoral cyanosis”, which is rare and suggests extensive thrombosis of the deep and superficial veins of the affected limb, accompanied by arterial spasm, and sometimes can lead to venous gangrene of the limb. The systemic symptoms are usually not obvious, the temperature does not rise above 39℃, and there may be mild tachycardia and acute discomfort.
Auxiliary examination
The following tests can be used to confirm the diagnosis of venous thrombosis that is difficult to diagnose.
(a) Upstream venography can understand the site and scope of thrombosis. The patient lies supine in a semi-erect position with the head end 30 to 45º. A rubber tube tourniquet is first tied around the ankle to compress the superficial vein. A 12-gauge puncture needle is used to directly percutaneously puncture into the superficial dorsal foot vein and inject 80-100 ml of 40% pantothenic glucosamine within one minute. Under the guidance of a TV screen, X-rays of the lower leg are taken first, followed by X-rays of the thigh and pelvis. After contrast injection, saline is then quickly injected to flush the venous lumen, reduce contrast irritation and prevent superficial phlebitis from occurring.
The contrast x-ray often shows spherical or sinuous filling defects in the veins, or the venous trunk is not visualized, and the distal veins are dilated and there are abundant lateral branch veins nearby, all of which suggest thrombosis in the veins.
(B) Vascular non-invasive examination method, in recent years, there has been great progress in the examination method for diagnosing deep vein thrombosis, using vascular non-invasive examination method, including radioactive fibrinogen test, ultrasonic examination, electrical impedance volume tracing method, etc. The radioactive fibrinogen test is more sensitive to check the calf deep vein thrombosis, and ultrasound examination is most valuable to check the iliofemoral vein thrombosis. If the above two examination methods are used, the diagnosis is not clear yet, and venography is still needed. So far, there is no non-invasive examination method that can completely replace the traditional venography. It is the direction of future efforts to continuously explore and improve the non-invasive examination method.
1. Radioactive fibrinogen test: The principle is 125 iodine labeled human fibrinogen, which can be taken up by the forming thrombus, formed by radioactivity, and can be scanned from the body surface. This test is simple to perform and has a high correct rate, especially for detecting smaller venous occult thrombi that are difficult to detect. Therefore this can be used as a screening test.
Its main disadvantages are: (i) it cannot detect old thrombus because it does not take up 125 iodine fibrinogen; (ii) it has a high false positive rate and is easily misdiagnosed. Therefore, it can only be used as a preliminary screening test.
2. Ultrasonic examination: The probe of ultrasonic detector is placed on the body surface position of larger veins of lower limbs, such as femoral vein, external iliac vein, middle superficial femoral vein, N vein and posterior tibial vein. The sound is made when blood passes through and disappears when there is no blood flow. This is an easy diagnostic method that can be repeated. A quick conclusion can be made. However, according to various reports, the confirmation rate varies from 31 to 94%. It has the following disadvantages: (1) it is not suitable for examining smaller venous thrombosis because it does not cause changes in blood flow in larger veins; (2) it is not easy to be detected if large veins are not completely disconnected; (3) if there are large side branches or superficial veins, it can cause the illusion of patency of deep veins; (4) it is not possible to measure thrombosis in the middle muscle veins, deep femoral veins and pelvic venous plexus.
3. Electrical impedance volume tracing method: the change of calf volume can be measured. In patients with lower extremity deep vein thrombosis, there is no obvious corresponding change in calf blood volume during deep breathing. This test can correctly diagnose thrombosis of larger veins, but the results are not satisfactory for thrombosis of smaller veins in the lower leg.
【Diagnosis
1. It is mostly 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, and the affected limb is swollen and hard and painful, which is aggravated after activity.
3. The thrombus site is painful, cords can be found along the blood vessels, the limb distal to the thrombus or the whole limb is swollen, the skin is blue-purple, the skin temperature is decreased, the dorsal foot and posterior tibial artery pulsation is weakened or disappeared, or venous gangrene appears. When the thrombus extends into the inferior vena cava, edema is evident in both lower extremities, buttocks, lower abdomen, and external genitalia. When the thrombus occurs in the muscular plexus of the lower leg, Homans’ and Neuhof’s signs are positive.
4. Late thrombus absorption mechanization, often leaving venous insufficiency, birth superficial varicose veins, pigmentation, ulceration, swelling, etc., called deep vein thrombosis after syndrome. Divided into: ① Peripheral type. Mainly blood backflow. ② Central type. Blood reflux disorder is the main type. ③Mixed type. There is both blood backflow and return obstruction.
5. Pulmonary embolism can be caused by thrombus dislodgement.
6. Radioactive fibrinogen test, Doppler ultrasound and venous hemogram are helpful for diagnosis. Venogram can confirm the diagnosis.
[Differential diagnosis
In the acute and chronic phases of lower extremity deep static thrombosis should be differentiated from the following diseases, respectively.
(a) Acute arterial embolism: This disease also often manifests as sudden pain of unilateral lower limb, which is similar to lower limb venous thrombosis, but there is no swelling of limb in acute arterial embolism, mainly manifests as cold skin temperature of foot and lower leg, severe pain, numbness, loss of voluntary movement and skin sensation, disappearance of dorsalis pedis artery and posterior tibial artery pulsation, and sometimes disappearance of femoral N artery pulsation, according to the above characteristics, it is easier to differentiate.
(2) Acute diffuse lymphangitis of the lower extremities: the disease also has a rapid onset, swelling of the extremities, often accompanied by chills, high fever, redness of the skin, elevated skin temperature, superficial veins without varicosities, according to the above characteristics, can be distinguished from deep vein thrombosis of the lower extremities.
(C) Lymphedema: this disease has similarity with the chronic phase of lower extremity deep vein thrombosis.
(D) Other diseases: acute calf myositis, acute calf fibrous histitis, calf muscle strain, bleeding calf deep vein rupture and Achilles tendon rupture. The latter all have a history of trauma, with an acute onset and severe local pain, accompanied by skin ecchymosis of the calf, especially the ankle, which can be differentiated.
For those who have difficulty in diagnosis, in addition to observation of clinical manifestations, one or two or more of the above special tests can confirm the diagnosis.
Treatment measures
(A) Acute stage: In recent years, the acute treatment of deep vein thrombosis is mainly non-surgical, but occasionally surgical treatment is still needed.
1. Non-surgical treatment
(1) Bed rest and elevation of the affected limb: Patients suffering from acute deep vein thrombosis need bed rest for 1~2 weeks to make the thrombus adhere tightly to the intima of the vein, reduce the local pain and promote the inflammatory reaction to subside. During this period, avoid squeezing to prevent the thrombus from dislodging and leading to pulmonary embolism. The affected limb should be elevated above the level of the heart, about 20-30 cm above the bed, and the knee joint should be placed in a slightly flexed position. If the elevation is appropriate, there is no need to use elastic bandages or wear elastic stockings. When you start to get up and move around, you need to wear elastic stockings or elastic bandages to moderately compress the superficial veins in order to increase the venous plus return flow as well as to maintain the minimum venous pressure and stop the development of lower limb edema. The use time of elastic stockings: ① for thrombophlebitis of deep or superficial veins of the calf, it is generally not needed, but if edema appears in the ankle and lower calf, it can be used for several weeks; ② for N and femoral vein thrombosis, it is generally used for no more than 6 weeks; ③ for iliofemoral vein thrombosis, it is used for 3 months first, and then removed intermittently, generally no more than 6 months, but if edema appears, it is necessary to continue to apply. Patients in the early stage, forbidden to stand and sit for a long time. For patients with heavy iliofemoral vein thrombosis, appropriate restriction of standing and sitting and elevation of the affected limb for 3 months can promote the establishment of collateral veins in the lower limbs to reduce lower limb edema.
(2) Anticoagulation: The use of anticoagulants can reduce the complication rate of pulmonary embolism and the sequelae of deep vein thrombosis. The effect is to prevent the continued growth of formed thrombus and the formation of new thrombus in other areas, and to promote the more rapid mechanization of thrombus.
Indications: ① within 1 month after the formation of venous thrombosis; ② when there is a possibility of pulmonary embolism after venous thrombosis; ③ after thrombectomy.
Contraindications: ① bleeding quality; ② after abortion; ③ subacute endocarditis; ④ ulcer disease.
Commonly used anticoagulants include heparin and coumarin derivatives.
Heparin is an effective anticoagulant with rapid efficacy, and can effectively control blood coagulation after 10 minutes of intravenous injection. It has a short duration of action and is rapidly destroyed in the body, mostly by enzymes and in small part by renal excretion. The blood coagulation time can be restored to normal after 3 to 6 hours of intravenous injection. It can be administered subcutaneously, intramuscularly, or intravenously. When heparin is applied, the coagulation time should be measured to adjust the heparin dose. The course of heparin is usually 4 to 5 days, followed by the application of oral anticoagulants, such as coumarins. Heparin generally has few allergic reactions. Excessive doses can cause bleeding, such as hematuria, traumatic bleeding or visceral bleeding. Once it occurs, it can be antagonized by fisetin sulfate at a dose of 1 to 1.5 mg against heparin 1 mg. It has a complete antagonistic effect and can be injected every 4 hours until the bleeding stops. Fresh blood can be transfused if necessary.
Coumarin derivatives are a thrombinogen inhibitor. It has a long induction period and usually takes 24 to 48 hours after administration before it starts to work. The effect also takes a long time to disappear, and there is a cumulative effect of drugs, and it often takes 4 to 10 days to completely disappear after stopping the drug. Coumarin derivatives are administered orally, generally, warfarin sodium is the most commonly used, 5mg on the first day, 3 times a day; 5mg on the second day, twice a day; 2.5mg or 5mg on the third day, once a day, adjusted according to the prothrombin time.
In case of bleeding caused by coumarin derivatives, the treatment is intravenous vitamin K110-20 mg. For severe bleeding, high-dose intravenous vitamin K1, 50 mg each time, once or twice a day, and fresh blood transfusion are required.
Where liver and kidney insufficiency and bleeding tendency, anticoagulation therapy is prohibited.
Anticoagulation course: 4-6 weeks for calf deep vein thrombosis; 3-6 months for iliofemoral vein thrombosis; 4-6 weeks for mild pulmonary embolism; 6 months for severe pulmonary embolism; coagulation function must be checked every two weeks during medication.
(3) Thrombolytic therapy: acute deep vein thrombosis or pulmonary embolism can be treated with fibrinolytic agents including streptokinase and urokinase within three months of onset. Streptokinase is extracted from the culture of Streptococcus haemolyticus, and urokinase is extracted from human urine, both of which are effective activators and can activate the fibrinogen in blood to convert it into fibrinase. This enzyme can hydrolyze fibrin into small molecule peptides to achieve the purpose of dissolving blood clots.
Urokinase administration method: Generally 100,000μ/time, dissolved in 5% glucose water or low molecular dextran 250-500ml intravenous drip, if necessary, twice a day, the course of treatment 10 – 14 days. Side effects: fever, nausea, vomiting, headache, lethargy, chest tightness and rash may occur, bleeding rarely occurs.
(4) Low molecular weight dextran:, is an adjuvant drug for the treatment of acute deep vein thrombosis, and is now widely used. Low molecular weight dextran can eliminate red blood cell coagulation, prevent thrombus from continuing to grow and improve microcirculation. The course of treatment is 10-14 days. It can be administered intravenously or simultaneously with heparin or urokinase. Side effects: Occasional allergic reactions, chest tightness, dyspnea, back pain, bleeding and chills, etc.
2. Surgical treatment: deep vein thrombosis of lower limbs is usually not surgically removed. However, for extensive iliofemoral vein thrombosis with arterial blood supply obstruction and the limb tends to gangrene (femoral cyanosis), surgery is often required to remove the embolus. The operation time of iliofemoral vein thrombectomy is usually within 72 hours after the onset of thrombosis, especially within 48 hours for the best results. The earlier the surgery, the less the thrombus adheres to the vein wall, the lighter the inflammatory response, the lighter the endothelial destruction, and the less the secondary thrombosis, the more complete the surgical thrombectomy can be and the better the postoperative outcome. Therefore, if we master the indications for surgery, iliofemoral vein thrombectomy is still one of the most effective treatment methods.
(2) Chronic phase: Within one year of the formation of deep vein thrombosis in the lower limbs, generally no venous reconstruction surgery is performed. During this period, a large amount of collateral circulation can be expected to be established. After medication and other adjuvant treatments, the venous reflux obstruction of lower extremity can be significantly reduced in many cases.
According to the pathological process, lower extremity deep vein thrombosis can be roughly divided into two phases: the obstructive phase and the recanalization phase, which are treated surgically in very different ways. Preoperative imaging of the superior and inferior deep veins of the lower extremities is required to clarify the location and extent of the lesion. Regardless of whether obstruction or recanalization is the mainstay, surgical treatment of the chronic phase of lower extremity DVT must be accompanied by medications and other adjuvant treatments. Different surgical options are appropriate for different sites, severity and stages of thrombosis. At present, various surgical methods have yet to be improved, and their efficacy has yet to be further improved.
Chinese medicine treatment】There are characteristics of Chinese medicine for the treatment of lower limb deep vein thrombosis. In the acute stage, it can diarrhea and cool the blood, or clear heat and cool the camp, and in the chronic stage, it can benefit the dampness and swelling or benefit the qi and spleen to open the ligaments. Chinese medicine is useful in relieving symptoms, anticoagulation, preventing thrombosis and pulmonary embolism, etc., and it is more effective when combined with western medicine.
Prevention
Preventive measures for acute lower extremity deep vein thrombosis include: operations around adjacent extremities or pelvic veins should be performed gently to avoid endothelial damage. Avoid postoperative pillows under the calf to interfere with calf deep vein reflux. Encourage frequent active movement of the patient’s feet and toes, and instruct more deep breathing and coughing movements. Get out of bed as early as possible and wear medical elastic stockings for the lower limbs if necessary. Special attention is paid to elderly, cancer or heart disease patients after thoracic, abdominal or pelvic greater than surgery, after femur fracture, and postpartum women. In addition, anti-platelet aggregation drugs such as Pansentine and enteric aspirin can be used to prevent lower limb deep vein thrombosis. Generally, the combination of Pansentine 25mg 3 times a day and enteric aspirin 0.3 3 times a day is used for better effect.