Deep vein thrombosis or DVT refers to the condition where blood clots form in the deep venous system of the body. Most commonly DVTs are found in the legs but they can occur in any vein including the abdomen (iliac veins and vena cava), the upper extremities (axillary and brachial veins), and the chest (subclavian veins, brachiocephalic veins, and superior vena cava).
It is estimated that DVT affects 250,000 patients annually in the United States alone, and DVT combined with pulmonary embolism accounts for 350,000 – 600,000 hospitalizations and 100,000-200,000 deaths per year.
The scariest thing about DVT and pulmonary embolism is that when these conditions occur, the presenting signs and symptoms may be vague, non-specific, or not even apparent at all. In some cases, the first symptom may be sudden death from an unsuspected massive pulmonary embolism. The diagnosis requires a high degree of suspicion and ability to associate subtle non-specific findings with potential risk factors. Because DVTs are often silent, if physicians even think about DVT as being a possible consideration, they will get an imaging study immediately to either confirm or exclude the diagnosis.
Clots form in the venous system as the result of three basic “environmental” conditions: stasis (slow or stagnant blood flow), endothelial injury (injury to the inside lining of the vein wall), and blood hypercoagulability (an excess capacity for blood cells to coagulate or stick together). If at least 2 of these conditions exist simultaneously, then blood has an increased tendency to form a clot.
Health conditions such as major fractures (hip or leg), major joint replacement surgery (hip or knee), major general surgery procedures, major trauma, and spinal cord injury are associated with a 10 times increase in developing a DVT. Conditions such as arthroscopic knee procedures, congestive heart or respiratory failure, cancer and chemotherapy use, hormone replacement (especially oral contraceptive use), pregnancy (or immediately after childbirth), paralytic stroke, inherited hypercoagulation syndromes (Factor V, Factor 20210, lupus anticoagulant, anticardiolipin antibodies, heparin induced thrombocytopenia (HIT), elevated homocysteine, and a family history of blood clots) or a previous history of DVT are associated with a moderate (2-9 times) increased risk of developing a DVT. Weak DVT risk factors (less than 2x increased risk) include bed rest more than 3 days, immobility due to sitting (such as prolonged car or air travel), laparoscopic surgical procedures, varicose veins, obesity, and increased age (typically considered age over 40).
Presenting signs of DVT may include warmth or redness in the area, leg pain, swelling or tenderness. If a DVT is suspected, the most commonly performed test is an ultrasound examination of the leg veins. Venous ultrasound is typically painless and non-invasive and uses sound waves to identify the vein, evaluate the venous blood flow, and image the clot itself. If a DVT is identified, then the appropriate treatment is anticoagulant therapy (blood thinners) to reduce the risk of clot extension, embolization, recurrence, and chronic valve damage (venous insufficiency). In selected patients with deep vein thrombosis affecting larger central veins in the abdomen, pelvis, arms, or chest, advanced therapy with medicines that actually “dissolve” blood clots (thrombolytic therapy) may be indicated. DVT patients who cannot be anticoagulated may be offered IVC Filter placement as an option to protect them from death or complications from pulmonary embolism.
Traditionally, anticoagulation therapy begins with a combination of 2 blood thinners: heparin and warfarin (Coumadin). Heparin has an immediate blood thinning effect, but can only be given by injection. Warfarin is given orally, but may take several days before adequate anticoagulation occurs. Once a therapeutic level of anticoagulation with warfarin is achieved (3-7 days) then the heparin is discontinued. Warfarin effectiveness is monitored by frequent blood test. The optimal range of “blood thinning” is to achieve an INR (international normalized ratio) of 2-3. Once started, anticoagulation continues for 3 months, and its further need is then reassessed. Occasionally, circumstances may dictate that the target INR might be either greater than or less than the 2-3 range but these decisions are individualized between the patient and their physicians, and represents balancing risk and benefit.
The primary risk of anticoagulation is bleeding. Risk is increased in patients over age 65, those with prior stroke, ulcer disease or GI bleeding, liver disease, diabetes, anemia, cancer, renal or heart failure, or combined with antiplatelet therapy (aspirin or Plavix). Major fatal bleeding events occur at a rate of about 0.2% per year.