Deep vein thrombosis (DVT) is a type of cardiovascular disease. DVT is a blood clot that forms in the large deep veins in the leg or pelvis area and grows toward the heart. Including the veins in the calf and thighs, the femoral, popliteal, and iliofemoral vein are also the sites of DVT development. It is a mainly common and dangerous condition (Kesieme et al., 2011). Some DVTs may cause no pain or swelling, whereas others might be quite painful and result in a lot of swelling. Mortality is not high with prompt diagnoses and treatment for most DVTs. However some can be a threat to your life, especially the ones that develop in the deep veins as compared to the clots that develop in the visible superficial veins. Clot which forms in the deep veins is more likely to break free and travel through the veins, which is then called an embolus. When an embolus travels from the legs or pelvis area and lodges into the lung artery, the condition is known as a pulmonary embolism or PE. This is a potentially fatal condition if it is not treated immediately and can lead to death. As high as 50% of the time a DVT can progress to pulmonary embolism. Collectively, DVT and PE are known as venous thromboembolism (VTE). DVT and PE are highly preventable (Kesieme et al., 2011).
Both DVT and PE are a major public health problem worldwide. DVT affects approximately 0.1% of persons per year. The overall average age and sex adjusted annual incidence of VTE is 117 per 100,000, with higher rates among men than women. For DVT, this accumulates to about 48 per 100,000. Males and females are both equally affected by a first VTE, however, men have a higher risk of recurrent thrombosis. Predominantly, DVT is a disease of the elderly (Kesieme et al., 2011). Approximately 600,000 people are hospitalized yearly with DVT’s in the U.S. (cdc.gov).
Alterations in hemostasis and blood coagulation are the process by which blood clots form. Hemostasis refers to stoppage of blood flow. It is designed to maintain the integrity of the vascular system. The process of hemostasis is divided into five phases: which are vessel spasm, formation of the platelet plug, blood coagulation, clot retraction, and clot dissolution (Porth, 2004).
Injury to the endothelial initiates vessel spasm. A spasm constricts the vessel and reduces the blood flow. It usually lasts less than one minute. A prostaglandin, Thromboxane A2 (TXA2), is released from the platelets, contributes to the vasoconstriction. Prostacyclin, is another type of prostaglandin, is released from the vessel endothelium, produces vasodilation, and inhibits platelet aggregation (Porth, 2004).
The second line of defense, the platelet plug, is initiated as platelets come in contact with the vessel wall. Platelets are large fragments from the cytoplasm of bone marrow cells called megakaryocytes. The platelets cytoplasmic granules release mediators for hemostasis. Additionally, platelets produce a growth factor that causes vascular endothelial cells, smooth muscle cells, and fibroblasts to proliferate and grow. Thrombopoietin is a protein that causes proliferation and maturation of megakaryocytes. Liver, kidney, smooth muscle, and bone marrow are the sources of thrombopoietin and they control platelet production. Platelet cell membrane is very important to its function. The outside of the platelet membrane is coated with glycoproteins that repulse adherence to the normal vessel endothelium, while causing adherence to injured areas of the vessel wall. The platelet membrane is also composed of glycoprotein receptors. Glycoprotein receptors bind fibrinogen and link platelets together. Furthermore, the membrane also contains large amounts of phospholipids that have a critical role in activating several points in the blood-clotting process (Porth, 2004). The formation of platelet plug involves adhesion and aggregation of platelets. Von Willebrand factor (vWF) is a protein that is required in the platelet plug formation. vWF is