Deep Vein Thrombosis

Topics: Coagulation, Deep vein thrombosis, Blood Pages: 11 (3653 words) Published: January 4, 2011
As a student nurse practitioner working within a medical assessment ward, I deal with a wide variety of patients who present with both acute and chronic conditions. This case study will identify the pathophysiology; look at the manifestations and clinical features of a condition. It will also discuss the therapeutic interventions and in turn evaluate the effectiveness of the interventions applied. Kyna (a pseudonym) was a forty-nine year old lady who was admitted to the ward for further investigations for a suspected deep vein thrombosis. She had never been in hospital before and had no medical or surgical history other than the fact that she was clinically obese, with a body mass index of 32, and had been attending her GP for hormone replacement therapy as she was post-menopausal. It was also identified that Kyna had just returned from New York where she undertook an eight-hour flight. A deep vein thrombosis can be described by Anderson et al. 1999 as a clotting of blood in a deep vein of an extremity. Weinmann et al 1994 states that a DVT is the result of a collection of intravascular cellular components, which consist of red, and white blood cells and some platelets bound together with fibrin strands. It usually occurs in the deep veins of the lower limbs as a result of slow blood flow and local activation of the blood clotting cascade and as a result of both local and systemic thrombogenic stimuli (Anand et al 1998). As discussed by Aquila (2001), in 1644, Schrnk first observed venous thrombosis when he described an occlusion in the inferior vena cava. In 1846, a German pathologist, Rudolf Virchow recognised the association between venous thrombus in the legs and PE. He formulated the Virchow triad, which found that venous stasis, vessel wall injury and hypercoaguable state all related to thrombus formation. In other words, the development of venous thrombosis is best understood as the activation of coagulation in areas of reduced blood flow. Each of these will now be discussed in detail. In relation to blood flow, thrombus formation occurs when the natural antithrombotic mechanisms are overcome. Furthermore, low pressures within the system complicate the haemodynamics. When a person stands upright, the hydrostatic pressure exceeds dynamic pressure impeding venous return. The action of the calf muscle pump overcomes this, which in turn can return the blood to the heart (Hirsch 1994). Laminar flow is also interfered with by clot formation. This promotes thrombus formation by bringing platelets into contact with the endothelium. Endothelial injury to blood vessels from a variety of sources is the most common cause of thrombus formation as stated by Cotran et al 1999. Porth 2005 goes on to explain that the endothelial layer provides a smooth and slippery inner surface for the vessel, which prevents platelet adherence and blood clotting as long as it remains intact. The endothelial cells produce prostacyclin, which produces a number of vasoconstrictor substances; plasmin and endothelium derived relaxing factors, all of which are important inhibitors of intravascular coagulation. A venous catheter can be used as an example of a source of vascular injury where the endothelial lining is disrupted, resulting in increased fibrin strands gathering at the site of injury, allowing a clot to form. Finally, hypercoagulability is the last element related to thrombus formation. White (2003) states that hypercoagulability is the condition in which an individual is at risk of but does not necessarily develop thrombosis. Basically, this means that it exists when coagulation overrides fibrinolysis. The coagulation pathway functions as a series of positive and negative feedback loops which control the activation process. In this case, the main aim of the pathway is to produce thrombin, which can then convert fibrinogen into fibrin, which in turn forms, a clot. Porth 2005 explains that the coagulation process results from the activation of...
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