I. Etiology
Deep venous thrombosis (DVT) is a venous reflux disorder caused by abnormal clotting of blood in the deep veins, mostly occurs in the lower limbs; thrombus dislodgement can cause pulmonary embolism (PE), the two together are called venous thromboembolism (VTE). thromboembolism (VTE). The DVT that causes PE usually comes from the large femoral or pelvic veins in the N fossa or more proximally, while the DVT distal to the lower extremity is less likely to cause PE.
DVT is most often seen in patients who are bedridden for long periods of time, after limb braking, major surgery or trauma, advanced tumors, or have a significant family history. Whereas DVT and PE are the most common causes of morbidity and mortality in orthopedic patients, in trauma patients, the presence of DVT will greatly complicate treatment, even beyond the impact of elective surgery, and if DVT and PE appear before the formal treatment of the fracture, the treatment modality must be adapted.
In addition to PE, complications of DVT include recurrent thrombosis and post-thrombotic syndrome (PTS), which is characterized by edema, sclerosis, pain, hyperpigmentation, ulceration, cellulitis, and stasis dermatitis, significantly affecting quality of life and even leading to patient death in severe cases.
In 1846, Virchow proposed the three elements of thrombosis, namely hypercoagulable state of blood, blood flow blockage and damage to the vessel wall. However, DVT occurs for a variety of reasons, often as a result of a combination of each other, and the main factors that cause thrombosis are as follows.
1.Slow venous blood flow Slow venous blood flow makes the blood have formed fraction especially leukocytes and platelets agglutinate in the peripheral layer of blood flow and gradually increase in size and deposit on the blood vessel wall to form thrombus. For example, patients who are bedridden for a long time, lower limb braking, and less activity of lower limbs after surgery will have sluggish venous blood flow, which may lead to thrombosis.
2.Venous wall injury Venous wall injury exposes the collagen fibers under the intima, which induces the activation of thrombinogen and platelet agglutination and promotes thrombus formation. For example, local muscle lacerations, fractures, venous valve repair surgery, etc., can cause mechanical damage to the vein wall, leading to thrombosis. And septic infection around the vein or in the vein lumen can also cause thrombosis.
3, blood hypercoagulation state The hypercoagulation state of blood is the basic factor of thrombosis. Surgery and trauma can stimulate platelet agglutination, estrogen and birth control pills can increase the vitality and quantity of coagulation factors, and endotoxin is released in sepsis, all of which can cause hypercoagulability of blood and thus make thrombosis easily.
At present, blood flow stasis determines the location of venous thrombosis, and the hypercoagulable state of blood may include both abnormalities of the coagulation and fibrinolytic systems, together with biological damage to the venous vascular endothelium; these three factors, in thrombosis, often act in combination. In this pathophysiological context, the lower extremity venous valves are reflected as an important factor in thrombosis.
Once formed at the valve pocket, early thrombi may adhere to the endothelium in the vicinity of the valve tip. These thrombi at the valve pocket then form on the structurally normal endothelium, causing a disturbance in luminal blood flow, and thrombus prolapse or retrograde spread can occur. And before the thrombus is firmly adhered to the vessel wall, it may fall off at any time to cause pulmonary embolism, a serious complication.
Prevention and treatment
1.Prevention
1.1 Primary measures In addition to the usual measures such as adequate hydration and analgesia, it is important to move early and use the limb actively, such as starting to move down to the floor as early as possible. For those patients who are immobile, the ankle should be repeatedly flexed and extended to promote venous blood flow. In addition, elevating the foot side of the bed may also increase blood flow velocity and reduce the risk of venous flow obstruction.
1.2 Physical Prophylaxis External physical measures include compression stockings, external inflation compression devices (EPCD), continuous compression devices (SCD), and arteriovenous foot pumps (AVFP). External compression reduces the cross-sectional area of the lower extremity and increases venous blood flow velocity. Compression improves venous lumen emptying and reduces flow blockage that can induce venous thrombosis. Studies have confirmed that compression compression stockings increase venous blood flow velocity by 30-40%, thus reducing the incidence of deep vein thrombosis. In addition to reducing blood stasis, these methods stimulate endothelial fibrinolytic activity. Most physical methods can be used in combination with anticoagulant therapy, as they have different mechanisms of action and do not have mutually antagonistic effects.
1.3 Drug prophylaxis As mentioned earlier, the hypercoagulable state of the blood is a major risk factor for DVT. Therefore, some anticoagulant drugs are used to prevent DVT. these drugs include common heparin, low molecular heparin, dextran and oral vitamin A antagonists.
2.Treatment: The aim of treating acute DVT is to prevent thrombus extension, early recurrence and death due to PE. In addition, long-term treatment should seek to prevent late recurrence and long-term consequences such as the development of PTS and chronic pulmonary hypertension.
2.1 Initial treatment
2.1.1 Anticoagulation: Drugs include common heparin, low molecular heparin, vitamin K antagonists, direct factor IIa inhibitors, factor Xa inhibitors, etc.
2.1.2 Thrombolysis The commonly used drugs include urokinase, recombinant streptokinase and recombinant tissue-type fibrinogen activator. And the methods of thrombolysis include catheter contact thrombolysis and systemic thrombolysis.
2.1.3 Surgical thrombus retrieval: It is an effective method to eliminate thrombus and can quickly release venous obstruction. The Fogarty catheter is commonly used to remove the iliac vein thrombus through the femoral vein, and the femoral N vein thrombus is removed by squeezing to expel the thrombus or by paralleling the thrombus.
2.1.4 Inferior vena cava filter placement: Inferior vena cava filters can prevent and reduce the occurrence of PE, but for most patients with DVT, routine application of inferior vena cava filters is not recommended because long-term filter placement may lead to inferior vena cava obstruction and a higher rate of recurrent DVT. Placement of an inferior vena cava filter is recommended only for those with contraindications or complications of anticoagulation therapy, or those at risk of PE despite adequate anticoagulation therapy.
2.2 Long-term treatment After initial treatment, patients with DVT require long-term anticoagulation to prevent the spread of thrombosis and/or recurrence of thrombosis. Anticoagulant drugs are usually vitamin K antagonists (e.g. warfarin) and direct factor Xa inhibitors (e.g. rivaroxaban). Other drugs such as flavonoids and hesperidin are also available to promote venous blood return, improve blood circulation and protect the vessel wall. In addition to pharmacological treatment, long-term use of compression stockings is recommended for patients in the chronic phase and, if available, limb circulation promotion devices can be used as an adjunct to treatment.