Comparing Chronic Venous Insufficiency and Deep Venous Thrombosis

Disorders of the Veins and Arteries Pathophysiology of Chronic Venous Insufficiency and Deep Venous Thrombosis Chronic venous insufficiency (CVI) pathophysiology is either the obstruction or reflux of venous blood flow (Gujja, Wiley, & Krishnan, 2014). The perforating veins valve normally functions by preventing the reflux of blood from the deep veins into the superficial veins. CVI occurs when there is venous hypertension that is caused by incompetent valves. Venous blood will escape from its normal antegrade flow path and it refluxes backward into the veins of an already congested leg.

After prolonged standing, the individual's veins will be completely filled and the venous valves will be flat open. This results in a high hydrostatic venous pressure due to the unbroken column of fluid that is extending from the head to the foot. The failed valves will cause the column of standing blood in the vein to remain high even during ambulation. Hydrostatic pressure will increase during and immediately after ambulation, which results in venous congestion.

Deep venous thrombosis (DVT) occurs when there are two of the Virchow's triad present in a patient. The triad consists of venous stasis, vessel wall injury, and altered blood coagulation (Prandoni et al., 2015). This triad will cause inflammation of the vein walls, which would eventually lead to thrombus formation. In response to the inflammation, venous thrombi are attached to the vein wall and they contain tail like attachment made of white blood cells, red blood cells, and fibrin.

It is possible for the tail to grow or spread in the direction of blood flow as the layers of clot are formed over time. This is critical since some of the blood clots might break off, travel in the blood stream and they end up blocking other veins. Venous thrombosis is the formation of a blood clot in a vein. While arterial thrombosis is the development of a blood clot in an artery.

Impact of Smoking on The Pathophysiology of CVI and DVT A smoker is more likely to suffer from DVT since smoking will make the blood cells stickier than they normally should and this results in them attaching to other blood cells resulting in clots. Smoking also alters fibrinolysis and this leads to blood clots not being destroyed normally. This increases the formation of blood clots. Smoking also harms the lining of the blood vessels. When the lining is destroyed, it becomes easier for clots to form.

For smokers, CVI will occur when there has been a blood clot blocking the flow of blood towards the heart, resulting in an increase in pressure in the vein that leads to the damage of the valves (Cepero, 2018). When the valves are damaged they will not be able to prevent reflux of blood, which results in increased blood pressure in the vein since no blood is flowing towards the heart. Diagnosing CVI one can use a Doppler to listen to the blood flow.

However, to get a more accurate examination, one should use the venous duplex ultrasound scan. This scan will offer an accurate image of the patient's vein (Katseni, Dimakakos, Bramis, Saatsakis, & Katsenis, 2017). A venogram can also be used to check on the flow of blood in the patient's veins and identify if there is any reflux. Diagnosing DVT begins with a physical examination that checks the patient's legs for any signs of DVT. Blood pressure, heart, and lungs of the patient are also checked.

Ultrasound can also be used to diagnose DVT (Swanson, 2015), and if the results are not clear, then a venogram is performed. DVT is treated by using anticoagulants. This will prevent the blood clot from getting bigger and prevents the blood clot from breaking off. Surgery can also be performed to remove the formed blood clots. CVI is treated by therapy, medication, or surgery. Therapy involves the use of compression socks that aid in relieving the pressure in the legs. The patient can also.