Virchow’s Triad — DVT and Blood Clots
There are three factors that are thought to contribute to deep venous thrombosis: an endothelial injury, venous stasis, and hypercoagulability. Deep venous thrombosis or blood clots from in the deep veins usually in the legs. Although deep venous thrombosis (DVT) predominantly occurs within the deep veins in the legs, it may also occur in the upper extremities. The deep veins pass through the deep tissues and the muscles. Muscle contractions — walking, running, or other activities — squeeze blood through the deep veins to the heart. The deep veins have valves which prevent the blood from flowing back to the feet and ankles.
DVT is the formation of a blood clot (thrombus) within a deep vein. The majority of blood clots that form are small and they are usually broken down or dissolved. Large clots may form and can block the vein causing the patient to complain of pain and swelling.
The clot may detach partially or totally (embolism). Some of the clots may be silent and show no symptoms. The detached blood clot may travel from the deep veins to the heart and then lodge itself in the pulmonary artery of the lungs. In some cases, the clot will pass through the heart to the aorta and create an emboli in the brain (patent foramen ovale). This contributes to the development of deep venous thrombosis. One of the factors in the triad may contribute more than the others. It is important to note that platelet dysfunction is not part of the Virchow’s Triad.
The first factor, Endothelial Injury, is secondary to injury or surgery and may occur due to manipulation of fractures, dislocations, or from the placement of retractors or pressure on the tissues. Endothelial injuries induce thrombosis.
Venous Stasis will lead to platelet contact with the endothelial lining such as with the use of a tourniquet, hypotension, or with knee flexion during surgery. It occurs with impaired mobility in the elderly. Immobility will cause the venous circulation to slow down and the clotting factors in the blood to clump together, ultimately leading to DVT. In my opinion, the most important factor to preventing blood clots is maintaining the patient’s mobility. It is important to get the patient up out of bed and moving around with possible — either on their own or with crutches. This is a simple preventative step.
The final factor in the triad — Hypercoagulability, can be affected by tissue debridement, collagen, fibrinogen, and tissue thromboplastin. Blood diseases such as Protein S and Protein C deficiencies are also important factors, as well as abnormalities in Factor V Leiden.
Risk factors for thromboembolism include a history of previous thromboembolism, obesity, malignant disease, immobilization, pregnancy, old age, history of congestive heart failure, and oral contraceptives. Other risk factors include genetic blood diseases — genetic hypercoagulable state and major orthopaedic procedures; up to 60% of asymptomatic DVT in total joint arthroplasty without prophylaxis, up to 20% of symptomatic DVT without prophylaxis, proximal DVT in about 15–25%, and fatal pulmonary embolism up to .05%. Total knee arthroplasties have a high risk of DVT, but a low risk of pulmonary embolism. When giving prophylaxis, balance the risk of clotting with the risk of bleeding.
