Deep vein thrombosis and pulmonary embolism are two aspects of one disease, and recently, there is a tendency to refer to both together as venous thromboembolism (VTE) [1]. Most of the foreign statistics on deep vein thrombosis originate from the 1970s and 1980s, and approximately 2 million people in the United States experience deep vein thrombosis and 600,000 people experience pulmonary embolism each year, of which 60,000 die. Deep vein thrombosis is a major comorbidity in orthopedic and major surgery patients, oncology and other chronic diseases.
From February 2003 to April 2003, 233 major surgery patients were enrolled in our anesthesiology department, and ultrasound examination was performed 3-10 days after surgery to find out whether deep vein thrombosis was formed. The incidence was 1.29%. The incidence was 49.29% in general surgery, 54.77% in thoracic surgery, 53.85% in neurosurgery, 47.2% in urology, and 35% in orthopedics. 39 patients (mainly orthopedic major surgery patients) who were anticoagulated with low molecular heparin had 43.59% (17/39) of DVT.
I. Etiology and risk factors of perioperative deep vein thrombosis
It occurs due to vascular injury, abnormal coagulation factors and local blood stasis. The natural coagulation, fibrinolytic factors and inhibitors present in the body are a complex balance in maintaining normal blood flow and hemostasis, and certain congenital or acquired changes in this balance system can make thrombosis easy to form.
(i) Causes of DVT due to surgery
(b) Vascular injury: surgical manipulation and position; thermal effect of bone cement in joint replacement surgery; thigh tourniquet.
Hypercoagulable state: hereditary hypercoagulable state resulting from the activation of exogenous coagulation system by tissue factor release after anesthesia and surgical trauma or defective coagulation inhibitory factors enhances coagulation.
Slowed venous blood flow: reduced preoperative activity; anesthesia and intraoperative immobilization; postoperative braking and prolonged bed rest; all slow down venous blood flow significantly
Major surgery, especially open chest, open abdomen, pelvic, lower extremity, neurosurgery and urology; trauma, especially pelvic or lower extremity fracture, acute spinal cord injury whether operated or not; pregnancy, childbirth, etc. at the same time there are three factors leading to DVT and the interaction accelerates DVT, is a high-risk patient of DVT.
(2) Risk factors leading to DVT in the perioperative period
Patients treated with preoperative medical drugs including malignant tumor, stroke, paralysis or long-term braking, myocardial infarction, congestive heart failure, respiratory failure and some infectious diseases are the causative factors of VTE, especially when there are congenital risk factors (see Table 1)
By evaluating these risk factors, the sixth American College of Chest Physicians (ACCP) in 2000, the risk stratification of preoperative and postoperative thrombosis can be classified as low, intermediate, high, and very high risk, and according to the risk stratification, active use of antithrombotic measures.
Pathophysiology of deep vein thrombosis
Venous coarse, low pressure, slow flow rate and low shear stress do not easily lead to platelet activation. The formation of venous thrombosis is different from arterial thrombosis, local blood flow stagnation plays an important role in the formation of thrombosis, and vascular injury is mostly the causative factor; the process of thrombosis is mainly the formation of thrombin with the participation of platelets, platelets are not the main component of thrombosis, and the corresponding treatment should be based on antithrombin.
The main danger of deep vein thrombosis is the acute pulmonary embolism caused by fragmentation and dislodgmentation; the dislodgmentation of large thrombus can lead to the patient’s immediate death, and the repeated dislodgment of small pieces can lead to the formation of chronic thromboembolic pulmonary hypertension. About 50% of pulmonary perfusion scans in patients diagnosed with deep vein thrombosis reveal pulmonary embolism, and 70% of symptomatic pulmonary embolism is accompanied by asymptomatic deep vein thrombosis. In addition, post-thrombotic syndrome (PTS) is very common as a result of thrombotic mechanization causing venous valve insufficiency or persistent obstruction, with a long-term follow-up incidence of proximal thrombosis in more than half and calf thrombosis in one-third. Common symptoms are leg swelling, calf pain, rare skin ulcers, and venous claudication, which affect work and quality of life [1,3].
Lower extremity venous thrombosis can involve superficial veins, deep calf veins and proximal deep veins, and different sites of thrombosis have significantly different prognosis. Superficial venous thrombosis is mostly benign, but may occasionally extend into the deep veins; compared with proximal deep vein thrombosis, the thrombus is smaller, mostly asymptomatic, and often completely autolytic, but proximal extension can be fatal. Large DVTs are rarely completely autolyzed, and less than 10% can be completely dissolved by heparin anticoagulation alone, which is the main source of emboli forming acute pulmonary embolism [1].
Deep vein thrombosis frequently begins in the lower leg, and by the time DVT causes symptoms, more than 80% have already involved the s vein or even higher (proximal DVT). About 20% of isolated calf DVTs extend to involve proximal veins within a week of onset, and 7% of calf DVTs cause pulmonary embolism, whereas proximal ones occur frequently [3].
III. Diagnosis of deep vein thrombosis
The clinical course of DVT is often insidious, and about 80% of DVT cases have no clinical symptoms, especially in the distal ones. Sometimes the first clinical manifestation of DVT is pulmonary embolism. Swelling and discomfort in the affected limb, unequal thickness of both lower limbs, pain and pressure along the veins, superficial varicose veins, skin dystrophy and chronic edema may be present in chronic cases.
Deep vein thrombosis is diagnosed by means of compression ultrasonography, venography and impedance plethysmography.
Color ultrasound vessels are not compressible and sound disappears, while normal compression and respiration have an effect on blood flow. The sensitivity of pressurized ultrasound imaging for the diagnosis of proximal venous thrombosis is more than 90%, the positive predictive value is greater than 90%, the accuracy is significantly higher than impedance volume tracing method, and it is a non-invasive test, which should be preferred.
Plasma D-dimer measurements have also been combined with pressurized ultrasound imaging or impedance volume tracing, and in non-surgical patients negative for both can rule out venous thrombosis [3]. Short-term D-dimer is almost always positive after surgery and should not be of great value for the diagnosis or exclusion of DVT, but can be used for preoperative DVT screening.
125I-labeled fibrinogen can be admixed to the thrombus for detection of developing thrombus and is used in many studies with little clinical utility [3-4]. Venography is diagnostically accurate, but is an invasive test and costly
IV. Prevention of deep vein thrombosis
Once thrombosis is formed, it often causes serious consequences, so prevention is better than cure. For the prevention of deep vein thrombosis, low molecular heparin is at least as effective as normal heparin and is more convenient to apply without monitoring [5]. Theoretically, it is best to start the drug preoperatively as primary prevention for surgery. European trials have mostly started preoperatively, while North America has mostly started application 12-24 hours postoperatively, mainly because of concerns about possible increased intraoperative bleeding and better thromboprophylaxis with European trials [6]. Prophylactic or therapeutic anticoagulation should be used with caution in all cases involving regional anesthesia or analgesia for spinal puncture or placement of an epidural catheter. Risk stratification for thrombosis should be performed preoperatively and postoperatively, and antithrombotic measures should be used aggressively according to the risk stratification. Physical or pharmacological methods or a combination of both can be used to prevent the formation of deep vein thrombosis.
1. Graded compression elastic stocking (ES): can be used alone or in conjunction with drugs
2. Intermittent pneumatic compression (IPC): can be used alone or in combination with graded compression stocking and/or drug therapy.
3. low-dose unfractionated heparin (LDUH): 5,000U twice a day, subcutaneous injection.
4.Low-molecular heparin (LMWH): subcutaneous low molecular heparin, higher dose for high-risk patients, about 4,000 U once a day, starting preoperatively or about 3,000 U twice a day, starting postoperatively; about 3,000 U once a day, starting postoperatively for intermediate-risk patients.
5. Warfarin: mostly started postoperatively with adjusted dose to INR2.0-3.0.
V. Treatment of deep vein thrombosis
The aim of treatment is not only to prevent thromboembolic events and thrombotic recurrence, but also to balance the risk it poses, i.e. the risk of bleeding.
(i) Heparin and low molecular heparin therapy
The treatment of deep vein thrombosis focuses on both the regulation of coagulation activity and the prevention of venous stasis. Once the diagnosis of DVT is established, continuous intravenous heparin or subcutaneous low-molecular heparin once or twice daily for about 1 week (5-10 days), if the patient has no abnormal bleeding, oral warfarin 3 mg starting within 24-48 hours after starting heparin therapy and adjusting the dose to INR 2.0-3.0 applied for at least 3 months, and graded compression stockings are the standard treatment for DVT method [2-4,6].
(ii) Direct thrombin inhibitors
Direct thrombin inhibitors (hirudin and its derivatives) are superior to common heparin in the prevention and treatment of deep vein thrombosis, and can be chosen especially in the presence of heparin-induced thrombocytopenia. Hirudin 15mg every 12 hours, subcutaneously for 7 to 10 days.
(iii) Thrombolytic therapy
Thrombolytic therapy is rarely used for postoperative deep vein thrombosis because of the definite efficacy of anticoagulation and the risk of bleeding associated with thrombolysis. According to a randomized trial, thrombolytic therapy may reduce the problems associated with post-thrombotic syndrome, and thrombolysis is currently limited to patients with extensive iliofemoral vein thrombosis [3-4,6]. Urokinase 2 million U, given intravenously over half an hour.
(iv) Vena cava strainer
Potential indications for vena cava filters are patients for whom anticoagulation is contraindicated (e.g., severe bleeding due to anticoagulation) or in whom anticoagulation has failed. Therefore, vena cava filtering is not recommended as a treatment for DVT [8].
(v) Incisional thrombectomy
Surgical incisional embolization was once recommended for proximal deep vein thrombosis occurring within 7 days; however, the recurrence rate after surgery is very high. There are not enough randomized trials to confirm its efficacy and safety, so its use is currently limited to giant venous thrombosis with limb ischemia [3-4,6].
VI. Deep vein thrombosis and pulmonary embolism
Common sources of emboli in pulmonary embolism include: proximal DVT of the lower extremity, distal DVT, pelvic thrombosis, renal/inferior vena cava thrombosis, and thrombosis of the right atrium and upper extremity venous system. Most pulmonary emboli originate from the deep veins of the lower extremities.
The incidence of pulmonary embolism is 7% for distal DVT and 70% for proximal DVT; distal DVT is mostly asymptomatic and proximal DVT is mostly symptomatic. The incidence of pulmonary embolism is 67% when the femoral vein is involved and 77% when the pelvic vein is involved. In severe pulmonary embolism, the thrombus is mostly present in the proximal end.
DVT often starts in the lower leg, and by the time DVT causes symptoms, more than 80% have already involved the s vein or even more proximal vein sites (proximal DVT). Approximately 20% of isolated calf DVTs extend to the proximal veins within a week of onset.
In patients with symptomatic proximal DVT, lung defects can be found in 50% to 80% of patients who have a lung perfusion scan.
The site of embolism: bilateral, multiple more than single, 57% bilateral, 42% unilateral; lower lung more than upper lung; right side more than left; recurrent occurrence may be common.
Unexplained and unexplained dyspnea and hypoxemia should occur after surgery, and syncope or sudden death in severe cases should be highly suspected of pulmonary embolism, and then further confirmed with ultrasound, spiral CT, pulmonary arteriography and isotope scan. Treatment of acute phase thrombolysis is the main focus, which can reduce the mortality rate of pulmonary embolism from 36% to 8%, while heparin anticoagulation.