The incidence of thrombus formation can increase in the presence of tissue trauma, blood stagnation or pooling, tissue irritation and/or rough areas found in the lumen of the vessel (McCance & Huether, 2002). Hypercoaguable states can occur in protein C deficiency, Factor 5 Leiden mutation, and elevated homocysteine levels and many other genetic abnormalities. Cancer, diabetes, smoking, prolonged immobility, and pregnancy are only a few of the environmental factors that increase the risks of clotting in the body (McCance & Huether). Use of certain medications can also cause hypercoaguablity. Birth control pills that contain estrogens can increase the risk of clot formation by 400% (Emanuele, 2004).
The presence of atherosclerosis of the vessels of the body is a common cause of thrombus formation without tissue trauma. Atherosclerosis in the vessel is characterized by the increase in collagen and smooth muscle fibers that have migrated into the tunica intima of the vessel lining. Deposits of cholesterol, lipids and plaque are permitted to collect and adhere to the inner lumen, thus reducing the inner diameter of the vessel and decreasing its ability to change size as needed.. These deposits also contribute to the hardening of the vessel by initiating an inflammatory response in which macrophages adhere to the tissues and release enzymes that further injure the vessels. The decreased lumen size causes shearing in the vessels, which can initiate the von Willebrand factor. This will then start the formation of a thrombus (Gibbins, 2004).
Treatment of thrombosis can differ dependent on the diagnosis of affected tissues. The primary goal is to restore blood flow to the affected are that may be blocked with the thrombus (McCance and Huether, 2002). In the case of an acute myocardial infarction or acute ischemic stroke, intravenous or intra-arterial thrombolytic therapy may be use if not contraindicated to assist in dissolve the thrombus (Fulgham, Ingall, Stead, Cloft, Wudicks, & Flemming, 2004).
Kikano and Brown have shown in their study that long term therapy with the use of an antiplatlet agent, such as aspirin is often beneficial in the presence of atherosclerosis (2007). Aspirin, even in low doses will inhibit the COX enzyme that is released by the activated platelet. This action will prevent the platelet from adhering to the vessel wall (Vorchheimer & Becker, 2006). After a cardiovascular event has occurred, the addition of an anti-coagulant such as heparin or Coumadin (warfarin) can be used. Heparin can be given intravenously or subcutaneously, and warfarin is taken orally. These medications interrupt the clotting cascade by speeding up the activity of the antithrombin III protein to stop the clotting process. Heparin, which is naturally produced by mast cells in the body, will halt the clotting process and actually increase the thrombin absorption by fibrin (McCance & Huether, 2002). Life-style changes such as diet, exercise and smoking cessation is critical to prevention of further complications related to thrombus formation (Kikano & Brown, 2007).
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