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Mechanisms, Diagnosis, and Treatment of Deep Venous Thrombosis

Deep venous thrombosis (DVT) is the third most common cardiovascular disease in the Untied States, and accounts for more than 250,000 hospital admissions and up to 200,000 deaths each year, according to David A. Cohen, MD, Thomas Jefferson University School of Medicine, Philadelphia, Pennsylvania, United States.

In a recently published overview of DVT, Dr. Cohen reviews the physiologic mechanisms leading to the DVT, as well as diagnostic strategies and treatment.

The major mechanisms leading to formation of DVT are stasis associated with surgical procedures or debilitating illness, hypercoagulability, and endothelial damage associated with leg trauma, any combination of which further enhances risk.

Patients with acute DVT commonly present with a red, swollen, painful leg, which may be confused with cellulitis. Areas of the leg are spared in cellulitis, however, while the erythema is confluent in DVT. Other conditions mimicking DVT are ruptures of either a Baker's cyst or the medial head of the gastrocnemius muscle.

The test of choice for DVT diagnosis is compression ultrasonography, in which the most accurate diagnostic criterion is the presence of a noncompressible segment of the common femoral or midpopliteal vein. Other tests include D-dimer assay and nuclear imaging with Technetium Tc 99 m apcitide, a small, synthetic, 13-amino acid peptide important in clotting.

Anticoagulation therapy with heparin and warfarin is indicated whenever DVT is diagnosed or suspected.

Unfractionated heparin may be administered intravenously according to a weight-based regimen, with a bolus of 80 units/kg body weight followed by an infusion of 18 units/kg/hour. Dosing of enoxaparin, a low molecular weight heparin (LMWH), can be either 1 mg/kg or 1.5 mg/kg administered twice daily.

Although unfractionated heparin and LWMH have comparable efficacy, LWMH offers a more predictable anticoagulant response. Additionally, LWMH is approved by the US Food and Drug Administration for outpatient use, lowering therapy cost.

Oral warfarin should be administered in conjunction with heparin therapy, starting with a maintenance dose of 5 to 7.5 mg.

The duration of anticoagulation therapy is dependent on the predisposing factor. DVT caused by a transient risk factor is adequately treated in 3 months. Idiopathic DVT should be treated for a minimum of 6 months. Patients with thrombophilic disorders should receive anticoagulation interminably.

Thrombolytic treatment regimens administered by catheter can clear thrombi more quickly than anticoagulant drugs, and can restore blood flow to the affected area, decreasing the risk of post-thrombotic syndrome.

In cases for which anticoagulation therapy is contraindicated, problematic, or insufficient, interior vena cava (IVC) filters may be used. Because of their association with DVT recurrence, however, IVC filters are best used as short-term or interim therapy when possible.
Hospital Physician 2003 April;18-22. "Deep Venous Thrombosis: An Overview"

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