Deep venous thrombosis (DVT) refers to the abnormal coagulation of blood within the deep veins, most commonly occurring in the lower extremities. Detached thrombi can lead to pulmonary embolism (PE). Together, DVT and PE are collectively referred to as venous thromboembolism (VTE), representing different stages of the same disease process.
Epidemiology, Etiology, and Pathogenesis
VTE is the third most common vascular disease after acute myocardial infarction and stroke, with an increasing annual incidence due to factors such as population aging. DVT primarily results from venous wall injury, blood stasis, and a hypercoagulable state. Hereditary risk factors include deficiencies in antithrombin, protein C, and protein S, as well as mutations such as Factor V Leiden and prothrombin gene mutations. Acquired risk factors include advanced age, a personal history of VTE, malignancy, and obesity. Triggering factors such as surgery, immobilization, pregnancy, and excessive estrogen exposure further increase the risk of DVT.
Pathology
Deep venous thrombi are primarily composed of red blood cells, along with small amounts of fibrin and platelets. The thrombi are only loosely attached to the vessel wall, making them prone to embolization and causing pulmonary embolism. Following the development of DVT, venous blood flow is obstructed, leading to distal tissue edema and hypoxia. Over time, this can progress to chronic venous insufficiency syndrome.
Clinical Manifestations
Based on the time of onset, DVT can be classified into three phases: acute (within 14 days after onset), subacute (15-30 days), and chronic (more than 30 days). DVT can also be categorized by location into proximal DVT and distal DVT. Proximal DVT involves the iliac, femoral, and/or popliteal veins, while distal DVT is confined to the deep veins of the calf.
Acute lower extremity DVT typically presents with sudden swelling and pain in the affected limb, accompanied by increased skin temperature, soft tissue tension, and localized edema with tenderness. When thrombi occur in the calf muscle venous plexus, a positive Homans sign (pain in the posterior calf muscles upon passive dorsiflexion of the foot) or a positive Neuhof sign (pain in the posterior calf muscles upon compression) may be observed. When thrombi obstruct the iliac or femoral veins and their tributaries, severe venous outflow obstruction can lead to extremely high tissue tension, compressing the arteries and resulting in limb ischemia. This may manifest as phlegmasia cerulea dolens (painful blue edema) or phlegmasia alba dolens (painful white edema). If untreated, shock and venous gangrene may develop.
In the chronic phase, particularly six months after onset, some patients may experience chronic venous insufficiency in the affected limb. Symptoms include swelling, pain, varicose veins, skin itching, hyperpigmentation, eczema, and ulcers, collectively referred to as post-thrombotic syndrome.
Diagnosis
The clinical manifestations of DVT are nonspecific, requiring auxiliary tests for diagnosis.
D-dimer
Elevated D-dimer levels are observed in DVT, with a sensitivity exceeding 95%, though specificity is low. Factors such as advanced age, inflammation, infection, and malignancy can also elevate D-dimer levels. A normal D-dimer level effectively excludes DVT.
Compression Ultrasonography
Compression ultrasonography is the first-line diagnostic method for DVT, with a sensitivity of up to 95% for thrombi in the popliteal vein or more proximal veins. For patients in whom venous ultrasound is inconclusive, alternative imaging modalities such as CT or MRI may be considered.
Venography
Venography has largely been replaced by ultrasound in clinical practice and is typically reserved for cases where interventional procedures are planned.
Treatment
The primary goal of DVT treatment is to prevent pulmonary embolism, especially in the early stages of the disease when the thrombus is loosely attached to the vessel wall and highly prone to detachment.
Bed Rest
Elevation of the affected limb above heart level is recommended until swelling and tenderness resolve.
Anticoagulation
For most cases of acute proximal DVT, anticoagulation therapy should be initiated promptly to prevent thrombus enlargement. Initial options for anticoagulation include heparin, vitamin K antagonists (e.g., warfarin), oral factor Xa inhibitors, and direct thrombin inhibitors. The specific choice is typically based on the clinician's experience, bleeding risk, patient comorbidities, preferences, cost, and convenience. When warfarin is selected as the long-term anticoagulant, it must overlap with heparin for 4-5 days to ensure adequate anticoagulation. The target for warfarin dose adjustment is maintaining the international normalized ratio (INR) between 2.0 and 3.0. Anticoagulation for acute proximal DVT should be continued for at least 3 months to prevent recurrence. For recurrent cases or those with persistent hypercoagulable states, such as malignancy, anticoagulation may be continued indefinitely.
Interventional Therapy
For patients with proximal DVT accompanied by severe limb swelling or ischemia, catheter-directed thrombolysis or percutaneous mechanical thrombectomy should be performed as soon as possible within 14 days after onset. If iliac vein stenosis greater than 50% is detected after thrombus removal, balloon angioplasty and/or stent placement may be considered.
Inferior Vena Cava (IVC) Filter
Placement of a percutaneous IVC filter may be considered to prevent pulmonary embolism in cases where anticoagulation is contraindicated, complications such as bleeding occur during anticoagulation therapy, VTE recurs despite adequate anticoagulation, or there is a large acute thrombus or a free-floating thrombus in the vein. IVC filter placement is also an option for patients with acute proximal DVT undergoing interventional therapy.
Prevention
At least half of newly diagnosed VTE cases in outpatients have a recent history of hospitalization, and many of these patients did not receive thromboprophylaxis during their hospital stay. Assessment of VTE risk in hospitalized patients is essential, and appropriate thromboprophylaxis should be provided when indicated.