Deep vein thrombosis (DVT) refers to the formation of clots (thrombi) in the lumen of deep vein vessels by blood components such as fibrin, platelets and red blood cells, and the normal flow of blood is blocked. Its incidence is high and its risk is great, and it is still prevention-oriented and combined with prevention and treatment.
I. Clinical symptoms.
Most symptoms of calf DVT are mild, mainly manifesting as pain and mild swelling in the calf, and pain when the dorsal foot is flexed or when the calf back muscles are compressed, which can generally ablate or autolyze with appropriate treatment. Ilio-femoral DVT may be confined within the deep iliac-femoral vein or may fill the deep veins of the entire lower extremity. The main clinical manifestations are swelling below the buttocks, angry superficial veins in the lower extremities, groin and affected abdominal wall, and increased skin temperature.
Once the blood clot breaks off from the vein wall, it moves with the blood flow and may attach to the lungs, causing an acute pulmonary embolism (PE). Large clots can dislodge to the point of immediate death, and repeated small dislodgements can lead to chronic thromboembolic (VTE) pulmonary hypertension.
In addition to the development of pulmonary embolism, DVT may also develop as a “sequelae of the affected limb”, with symptoms such as edema, lower leg hyperpigmentation, venous ulcers, and limb disability, etc. The swelling, distension, and pain in the legs caused by DVT are usually single-limb disorders, with the left lower limb being the most common. The onset of leg swelling, distension and pain is relatively sudden, and about half of the patients do not have any symptoms.
Second, high-risk factors.
1. The basic elements of thrombosis, namely the Virchow triad: hypercoagulable state, endothelial injury and venous stasis. There are unique reasons for the high incidence of VTE in orthopaedic surgery.
(1) After lower extremity arthroplasty and hip fracture surgery, blood clotting is likely to occur due to the presence of tissue fragments, collagen, and fat in the blood; peripheral V dilatation due to crestal or general anesthesia during surgery; muscle paralysis; and slow blood flow due to postoperative pain and bed rest.
(2) Distortion of blood vessels during lower extremity surgical operations and damage to the vessel wall from bone fragments increase the probability of endothelial cell injury.
(3) The use of thigh tourniquets during total knee arthroplasty, prolonged knee flexion, postoperative immobilization, decreased mobility, postoperative local swelling and limited mobility increase venous stasis. As well as major surgery causes enhanced platelet adhesion in hypercoagulable form; postoperative serum pre-fibrinolytic activator and fibrinolytic enzyme both have elevated inhibitory levels, resulting in reduced fibrinolysis.
2. High risk factors include obesity, diabetes, hyperlipidemia, hypertension; taking contraceptive pills, pregnancy, old age, smoking, surgery, trauma, previous history of VTE, paralysis, braking, sedentary, prolonged lying, intraoperative application of tourniquet, general anesthesia, malignancy, central venous cannulation, chronic venous insufficiency, etc. Among them, major orthopedic surgery is also a high risk factor for VTE.
Third, examination and diagnosis.
1, plasma D-dimer measurement. D-dimer is a cross-linked fibrin degradation product, which only appears when fibrinogen formation and decomposition are in a stable state. if plasma D-dimer concentration >500μg/L is used as the positive threshold value for diagnosing vascular embolism, it has good sensitivity (98%) for judging pulmonary embolism. It also maintains a high sensitivity after 3 and 7 days (96% and 93%), but its specificity is not high because many diseases can be associated with fibrin formation and degradation: for example, myocardial infarction, tumors, infections or inflammatory diseases. Its specificity for the diagnosis of pulmonary embolism is also influenced by age: studies have shown that the specificity of D-dimer for the diagnosis of pulmonary embolism is 72% in people aged 30-39 years, while it is only 14.3% in people older than 70 years. The diagnostic value of D-dimer in vasoembolic disease has yet to be determined, and most studies suggest that plasma D-dimer ≤500 μg/L can basically exclude the diagnosis of pulmonary embolism. However, a plasma D-dimer of ≥500 μg/L is only highly suggestive of the possibility of vascular embolism, but not sufficient to confirm the diagnosis of pulmonary embolism. In addition, blood lipids, blood glucose and blood flow should be tested.
2, preoperative and postoperative lower limb A/V ultrasound; upstream venography, venous pressure measurement, etc.
IV. Preventive measures.
1.Basic precautions
(1) Operate gently and delicately to avoid damaging the endothelium of the vein.
(2) standardize the use of tourniquet.
(3) postoperative elevation of the affected limb to prevent deep venous reflux obstruction.
(4) Educate patients about prevention of venous thrombosis, encourage patients to turn over regularly, early functional exercise, early movement of feet and toes, getting out of bed, and deep whistling and coughing movements; if necessary, wear medical elastic stockings or electrical stimulation of lower limbs to accelerate venous blood flow.
(5) Intraoperative and postoperative moderate rehydration, to avoid dehydration and increase blood viscosity.
(2) The coagulation process continues to activate for up to 4 weeks after major orthopedic surgery, and the risk of postoperative DVT can last up to 3 months. Compared with artificial total knee arthroplasty, artificial total hip arthroplasty requires a longer time frame for anticoagulation prophylaxis after surgery. Therefore, the time frame for DVT prophylaxis after major orthopaedic surgery is generally not less than 7-10 d, and can be extended to 28-35 d if necessary. The high incidence of perioperative DVT in major orthopaedic surgery is 12-24 h after surgery. At one stage, DVT does not have obvious clinical manifestations, but the consequences are serious, and prophylaxis of DVT should be performed as early as possible. Low molecular heparin sodium 2500u subcutaneously (H) 1 time/day (qd ) for 5~7 days before surgery. If rivaroxaban is used, it can be given orally for 35 days until DVT is less likely to occur. If you use “Speedy Lin” 0.3ml (2850iu)/day for 10 days, 12h before and after the start of surgery, or 2h before surgery.
V. Acute phase treatment.
Once DVT is formed, drug therapy is preferred in the acute phase, and surgery or other treatment methods will be considered only in very few special cases (fear of thrombus dislodgement should be put in the filter before surgery). For example, for patients with objective evidence of DVT
(1) Initial short-term treatment with subcutaneous low-molecular- weight heparin ( LMWH) or intravenous/subcutaneous heparin (Heparin) is recommended for a course of at least five days in combination with the vitamin K antagonist warfarin (Warfarin), and after five or six days heparin is discontinued and warfarin is continued. This drug therapy is called anticoagulation. Anticoagulation is an important treatment for DVT. Anticoagulants do not dissolve the clots that have formed, but they prevent the blood clots from continuing to develop by prolonging the clotting time. Warfarin is generally taken until the patient resumes normal activity, and then maintenance therapy continues for a period ranging from 3 to 6 months.
(2) Thrombolysis: for patients within one week of onset, fibrinolytic agents including streptokinase and urokinase can be applied; pulmonary embolism (PE) can be extended to 14 days; cerebral thrombosis 3-6 hours is the golden time. In short, the earlier the thrombolysis, the better.
(3) Bed rest for 1-2 weeks during the acute period (to make the thrombus stick to the endothelium, anti-inflammation and pain relief), with the affected limb elevated at the level of the heart (20-30cm from the bed).