Deep vein thrombosis
A thrombus forming in a deep vein most commonly within the lower limb.
Increased risk of thrombosis may result from blood stasis, vascular damage or hypercoagulability (Virkoff ’s triad).
· Venous stasis: Immobility, obesity, pregnancy, paralysis, operation and trauma.
· Intimal damage: Trauma to a vein, e.g. after a hip operation, can provide a starting point for thrombosis.
· Thrombophilia: Factor V Leiden, antithrombin III deficiency, protein C and protein S deficiency, drugs including the combined oral contraceptive pill.
Other risk factors include increasing age, malignant disease, varicose veins and smoking.
The starting point for thrombosis is usually a valve sinus in the deep veins of the calf, primary thrombus adheres and grows until flow is occluded. Secondary thrombus forms which then progresses proximally.
The condition is often silent and pulmonary embolism may be the first sign. Calf pain with swelling, tender-ness, redness and engorged superficial veins are com-mon. Clinical examination alone is unreliable for diag-nosis.
Pulmonary embolism is a serious complication and may be life-threatening, particularly when the embolus is large, e.g. when it arises from the iliofemoral segment.
Ultrasound or Doppler ultrasound scans can be used to confirm the diagnosis; below-knee thromboses cannot be easily seen and may only be diagnosed with venography. Alternatively, in patients with a low clinical risk for deep vein thrombosis may be screened using the D-dimer test. If the D-dimer is normal no further investigation is required.
Bed rest and compression stockings; patients with above-knee thromboses should be initially anti-coagulated with low-molecular-weight heparin and then converted to warfarin for 3 months with the INR maintained between 2 and 3. Thrombolytic therapy is occasionally used for patients with a large iliofemoral thrombosis.
Prophylactic low molecular weight heparin should be given to patients with immobility due to cardiac failure, or surgery to the abdomen, leg or pelvis.
Destruction of deep vein valves occurs in half of patients, with the development of chronic venous insufficiency.
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