This paper explores the epidemiology, pathophysiology and clinical manifestation of Chronic Venous Thrombosis (CVI) and Deep Venous Thrombosis (DVT). In the paper, the pathophysiology and clinical features of the two conditions are compared and contrasted. The patient factor of behaviour and lifestyle has been selected to discuss the two conditions.
Pathophysiology of CVI and DVT: Similarities and differences:
Chronic Venous Insufficiency is a condition associated with the compromise of venous blood flow due to a longstanding venous hypertension, which results from functional abnormalities of structural changes in the veins and the valves (Lijfering et al., 2011). Although it may have different causes, chronic venous insufficiency develops, as a result, of high venous pressures. When veins become diseased due too thrombus, age, genetic predisposition, trauma or idiopathic factors, the competence of the veins to decrease pressures decreases greatly. In essence, the venous pressure in diseased veins decreases during ambulation by only 20% instead of the normal 70% (Lijfering et al., 2011). As a result, there is a significant effect on the normal antegrade blood flow from the leg to the heart. The condition affects the high pressure deep veins, low pressure superficial veins and also the connecting veins. It is aggravated by age, obesity, gender, family history of phlebitis, and deep venous thrombosis.
Deep venous thrombosis, on the other hand, is a condition associated with the formation of a thrombus in the venous system (hypercoagulability), the injury of the veins or venous stasis. The thrombus form in one or more of the body’s deep veins, especially the leg veins. In som instances, the progression would be facilitated by inflammation or, in other cases through phlebothrombosis. The development of the thrombus compromises the back flow of blood to the heart (Rajagopalan,Mukherjee, &Mohler, 2011).
Venous and arterial thrombi are different. Arterial thrombosis develops where plaques form, while venous thrombi develop at the points where the veins are not damaged. Additionally, arterial thrombi develops at points where shear stress is high, unlike venous thrombus which develops at points of low shear stress (Hallet, Brewster, &Russmussen, 2001).
Both CVI and DVT are mostly associated with the venous system. They share some causative factors such as gender, age, family history of disease and behavior or lifestyle. Additionally, the two conditions mostly affect the legs. However, DVT is a causative factor for CVI. A diagnosis of DVT is a risk factor for CVI. Further, DVT progresses, as a result of thrombus formation, while CVI is directly linked to the development of high venous pressure.
Patient Factor, Effect on Pathophysiology and Prescription of Treatment:
The factor I identified that affects pathophysiology of CVI is lifestyle or behavior. As regards CVI, a behavior like prolonged standing, or even sitting position at work leads to difficult in backflow of blood because of gravity. This leads to a build of high venous pressure in the legs leading to CVI. Similarly, long periods of sitting may compromise the back-flow of blood, precipitating the development of a clot, leading to DVT.
Based on the patient factor of longstanding and long hours of sitting, I would first ascertain the sitting hours of the patient under consideration, in order to link the lifestyle to the condition. For example, a client with a history of long hours of sitting, while working on a computer, may present with legs discomfort, varicose veins, edema of the legs, hyperpigmentation and static dermatitis (Yadava, 2013). In addition, the client can present with cutaneous infarction or venous ulceration. Such clinical manifestations may be pointing to a venous disease as CVI or DVT. Diagnostic measures like D-Dimer testing and coagulation studies would be used to differentiate the conditions. Based on the causative factor of long hours of sitting, I would prescribe treatment that requires the client to change the lifestyle. I would prescribe regular exercises, regular breaks every hour, rotating on the seat on the ankles and regularly stretching the calf muscles to prevent the progression.
Hallet, W. J., Brewster, C. D., &Russmussen, E. T. (2001). Handbook of patient care in vascular diseases. Volume 186, volume 2001. Hoboken, NJ: Lippincott Williams & Wilkins.
Lijfering, W. M., Flinterman, E. L., Vandenbroucke, P. J., Rosendaal, F., &Cannegieter, C. S. (2011). Relationship between venous and arterial thrombosis: a review of the literature from a casual perspective. Seminars in Thrombosis and Hemostasis, 37(8), 885-896.
Rajagopalan, S., Mukherjee, D., &Mohler, R. E. (2011). Manual of vascular diseases. Hoboken, NJ: Lippincott Williams & Wilkins.
Yadava, P. O. (2013). Deep vein thrombosis-ECAB. Philadelphia, PA: Elsevier Health Sciences.
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