What is deep vein thrombosis?

Causes and Symptoms

Deep vein or venous thrombosis (DVT) is a blood clot (thrombus) in a deep vein. In vessels that transport blood toward the heart, various disorders including skin infections or phlebitis
(inflammation of the vein) can occur; however, specific tests are required to diagnose the existence of DVT. While phlebitis afflicts superficial veins, DVT occurs in deep veins, usually in the legs.

Because of the possibility of its breaking loose, lodging in the lungs, and creating a potentially fatal pulmonary
embolism

(blockage of blood to the lungs), a clot in the leg is highly dangerous. Clots in veins in the legs generally form following long periods of inactivity or lengthy bed rest, pregnancy, obesity, smoking, estrogen therapy, oral contraceptive medication, or surgery.

With DVT, the afflicted leg begins to swell, turn red, become warm, and throb. Occasionally, the area is tender to touch or movement. However, about one-half of the instances of DVT produce no symptoms, and it is frequently referred to as a silent killer.

Treatment and Therapy

Treatment for deep vein thrombosis begins with anticoagulants (blood thinners), specifically heparin, administered intravenously in the hospital, or through self-injections given at home. The anticoagulant warfarin (Coumadin), given as pills, are then prescribed daily to prevent clots from becoming larger. Frequent check-ups with a physician are mandatory to maintain a certain level of medication effectiveness; depending upon the risk of further clotting, Coumadin can be required anywhere from three months to the remainder of the patient’s life. Patients may also be advised to elevate the afflicted leg or apply a heating pad to the area. Walking is sometimes recommended, as is wearing tight-fitting stockings or compression stockings to reduce pain and swelling. In the event that Coumadin is unable to prevent blood clots, a filter may be surgically placed into the vena cava, the large vein carrying blood from the lower body to the heart, to prevent clots from entering the lungs. Also, a large clot may be removed through surgery or may be treated with powerful clot-destroying drugs.

Perspective and Prospects

Inquiries into the mysteries of blood coagulation have existed since 400 BCE, when Hippocrates observed that blood appeared to congeal as it cooled. By the nineteenth century, Pierre Andral, the founder of hematology (the branch of biology that deals with the blood and the blood-forming organs) and one of the first physicians to study the chemistry of the blood, formulated the classical hypothesis of blood coagulation. He found that the process of blood coagulation follows two pathways: the intrinsic, wherein, within seconds, platelets form a hemostatic plug at the site of the injury (primary hemostasis, or stoppage of bleeding); and the extrinsic, wherein fibrin molecules react in a complex cascade or network (secondary hemostasis) that ultimately moves into a third stage, wherein protein factors combine with the enzyme thrombin and contribute to the clotting of blood. Twentieth-century research determined, however, that the tissue pathway (formerly known as the extrinsic) is a series of enzymes generated to participate with thrombin and catalyze fibrinogen into fibrin, which is essential to blood clotting. These factors are responsible for any abnormalities in the clotting of blood.

While the most commonly known blood clotting disorder is hemophilia, or uncontrolled bleeding, its opposite condition, hypercoagulation, specifically the formation of abnormal clots in veins, can also be life-threatening. In 1994, the clotting disorder factor V Leiden (named for the Dutch city in which it was discovered) was identified as a hereditary resistance to activated protein C. An estimated 30 percent of those individuals who suffer from hypercoagulation are afflicted by this enzyme mutation that encourages the overproduction of thrombin and, consequently, causes excessive clotting. Most of these persons are unaware of their condition or its dangers. Treatment and control of this disorder depends largely on antiplatelet medication, such as aspirin or clopidogrel (Plavix), that is designed to prevent platelets from sticking together. Maintaining a heart-healthy lifestyle by getting regular caradiovascular exercise, maintaining a healthy weight, avoiding smoking, and controlling blood pressure and cholesterol levels can significantly reduce an individual's risk of developing lethal blood clots.

Continued research into the complexities of coagulation account for new developments in medications, including thrombin inhibitors or molecular products that target enzymes controlling specific coagulation factors.

Bibliography:

American Medical Association. Family Medical Guide. 4th ed. New York: John Wiley, 2004.

"Are You at Risk for Deep Vein Thrombosis?" Centers for Disease Control and Prevention, March 7, 2011.

"Fact Sheet: Deep Vein Thrombosis and Pulmonary Embolism." SurgeonGeneral.gov, n.d.

Johnston, Bernard, ed. Collier’s Encyclopedia. 24 vols. New York: Collier’s, 1997.

Owen, Charles A. History of Blood Coagulation. Edited by William L. Nichols and E. J. Walter Bowie. Rochester, Minn.: Mayo Foundation for Medical Education and Research, 2001.

"What Is Deep Vein Thrombosis?" National Heart, Lung, and Blood Institute, October 28, 2011.

Wood, Debra. "Deep Vein Thrombosis." Health Library, May 7, 2013.