Chronic venous insufficiency is a term used to describe the functional abnormalities of the venous system or the multiple manifestations of the chronic venous disease. Chronic venous Infection (CVI) is a common disorder affecting at least 25 percent of the adult population and is associated with multiple impacts on socioeconomic and patients’ quality of life, especially due to treatment costs and irreversible sequelae promoted by the condition and venous leg ulcers (Santler & Goerge, 2017). The clinical manifestations of the disorder include leg edema, lipodermatosclerosis, which is a sign of impending ulceration. On the other hand, deep vein thrombosis (DVT) encompasses a subset of venous thromboembolism (VTE) (Stone et al., 2017). Compared to chronic venous insufficiency, DVT is also associated with high morbidity and mortality rates, in particular resulting from pulmonary embolism (PE), which is a dreaded complication of DVT. The incidence of VTE is estimated to be about 1 per 1,000 individuals every year, with deep vein thrombosis accounting for two-thirds of the events. The clinical manifestations of the deep vein thrombosis include leg swelling, leg pain, and venous ulcers in severe cases. In light of this, we compare the pathophysiology of chronic venous insufficiency and deep thrombosis and expound further to distinguish between venous thrombosis and arterial thrombosis. In addition, we analyze and present how the patient factor might affect the pathophysiology of CVI and DVT, as well as, diagnosis and treatment of the two disorders.
Pathophysiology of Chronic Venous Insufficiency and Deep Vein Thrombosis
Drawing upon existing literature, several studies suggest that the pathogenesis of the chronic venous disease is caused by reflux (backward flow) or obstruction of venous blood flow. To understand the pathophysiology of CVI, it is important to understand the anatomy and the function of the normal venous system from the legs to the central circulation. From the legs to the central circulation, blood must flow upwards against the gravity from the lower extremity venous system to the central circulation – the heart. The veins contain a one-way valve, and when damaged, blood leaks backward leading to a backward flow of the blood in the legs. When this happens, it becomes hard for the blood to flow from the legs to the heart, alongside increasing blood pressure in the veins, which causes CVI. Focusing on backward venous flow Santler and Goerge highlighted that reflux or backward flow is based on several mechanisms, but the major players are the venous valve incompetence, hemodynamic factors, venous hypertension, and vessel wall inflammation. The same was supported by a study by Eberhardt and Raffetto (2014), which indicate that valvular incompetence of the superficial veins or the axial deep, perforator veins, venous tributaries, or a combination of all mechanisms causes backward flow. Alongside the reflux or the backward flow, obstruction of the deep veins is associated with the development of chronic venous insufficiency. As elaborated by Eberhardt and Raffetto, obstruction of the deep veins is known to limit blood outflow leading to increased venous pressure with muscle contractions, which results in secondary dysfunction of the muscle pump. The failure by the muscle pumps has the potential to lead to ineffective discharge of venous blood from the distal lower extremity leading to post-ambulatory venous pressure, which is nearly as high as the pressure associated with a prolonged erect position.
On the other hand, deep vein thrombosis is associated with three contributing factors – venous stasis, vascular injury, and hypercoagulability. According to Stone et al. (2017), venous stasis is the most consequential, although it has been identified to be insufficient to lead to the formation of a thrombus. Stone et al. note that the simultaneous presence of venous stasis alongside vascular injury or a hypercoagulability increases the risk of clot formation. Venous thrombosis occurs in areas with a low or mechanically altered flow of blood such as areas adjacent to valves in deep veins. Studies indicate that valvular reflux may be considered as a risk factor for DVT as a significant number of patients with DVT have pre-existing primary chronic venous insufficiency (Shaydakov, Comerota, & Lurie, 2016). Evidently, the two disorders are caused by the incompetence of the venous system – with CVI being caused by damaged valves and DVT caused by blood clot in the veins.
Venous Thrombosis vs. Arterial Thrombosis
Venous and arterial thrombosis is considered as separate pathophysiological entities (Prandoni et al., 2015). More specifically, arterial thrombosis is largely associated with platelet activation, while venous thrombosis is inclined towards activation of the clotting system. The risk factors for venous thrombosis have been identified as obesity, age, diabetes mellitus, hypertriglyceridemia, and blood hypertension. On the other hand, a few markers of arterial thrombosis have been identified including sex, age, and arterial hypertension.
Impact of Patient Factor on the Pathophysiology of CVI and DVT
The patient factor identified is age for both the pathophysiology of CVI and DVT. Studies indicate that the incidence of deep venous thrombosis exponentially increases with age. Elderly patients predispose higher incidences of immobility, comorbidities, and hypercoagulability due to aging (Raghid, 2014). Advanced age has been identified as an independent risk factor for VTE, which is related to deep vein thrombosis. Along with that, age has also been associated with increased risk of chronic venous insufficiency (Vuylsteke et al., 2015). With old age comes along a decrease in collagen and elastin, which has the potential to contribute to decreased venous compliance.
Diagnosis and Treatment of CVI and DVT
The diagnosis for chronic venous infection is based on clinical presentation, patient medical history, and diagnostic tests (Sentler & Goerge, 2017). The duplex ultrasound is currently the gold standards, although other diagnostic procedures may be used under certain circumstances. For instance, use of Doppler and duplex ultrasound allows for exploratory and inexpensive examination of the veins in the legs to look for acoustic signals that are likely to cause venous blood flow. Treatment of chronic venous insufficiency is both conservative and invasive. The goal of the two forms of treatment is to prevent the sequelae and complication of CVI and promote ulcer healing. Some of the conservative treatment options include compression therapy and supportive procedures such as manual lymphatic drainage and physical therapy. Compression therapy is the most preferred, but should only be used in patients with advanced CVI. If otherwise, compression therapy should be combined with surgical and endovenous procedures. Sclerotherapy and phlebectomy are used in the treatment of isolated tributary or perforator incompetence or recurrent varicose veins.
On the other hand, the diagnosis of deep vein thrombosis uses diagnostic imaging to check for the presence of DVT (Stone et al., 2017). Ultrasound is the most preferred imaging modality because it is easy to use, safe, cost-effective, and reliable. During the diagnostic procedure, the ultrasound attempts to compress the vein, and failure to compress reflects diagnostic for DVT. Afterward, a duplex such as a color-flow Dopler is used to characterize the clot. Contrast venography is currently the gold standard for lower extremity deep vein thrombosis. Treatment of deep vein thrombosis involves the use of anticoagulation therapy. Except for a few patients, a majority of patients with deep vein thrombosis can be treated with oral anticoagulants alone. However, for patients with extensive thrombus burden with proximal deep veins, the recommended treatment option is the use of mechanical and catheter-directed thrombolysis to induce clot lysis and minimize the risk of post-thrombotic syndrome.
Both chronic venous insufficiency and deep vein thrombosis are common disorders caused by the complication in veins. In particular, CVI is caused by venous reflux and obstruction, while DVT is caused by blood clot in deep veins. Although the pathophysiology of the two disorders is different, the diseases are associated with considerable complications and socio-economic burdens among other challenges. Early detection and proper diagnosis of the disorders is important for the proper treatment of the diseases.
Chronic Venous Insufficiency Ming Map
Deep Vein Thrombosis Mind Map
Eberhardt, R. T., & Raffetto, J. D. (2014). Chronic Venous Insufficiency. Circulation, 130, 4, 333-346.
Prandoni, P., Milan, M., Vedovetto, V., Sarolo, L., Adamo, A., & Bilora, F. (2015). Venous and Arterial Thrombosis: Is there a Link? International Journal of Hematology Research, 1(2), 29-34.
Raghid, K. (2014). Influence of Acquired and Genetic Risk Factors on the Prevention, Management, and Treatment of Thromboembolic Disease. International Journal of Vascular Medicine. dx.doi.org/10.1155/2014/859726.
Santler, B., & Goerge, T. (2017). Chronic venous insufficiency – a review of pathophysiology, diagnosis, and treatment. Jddg: Journal Der Deutschen Dermatologischen Gesellschaft, 15(5), 538-556.
Shaydakov, M. E., Comerota, A. J., & Lurie, F. (2016). Primary venous insufficiency increases risk of deep vein thrombosis. Journal of Vascular Surgery: Venous and Lymphatic Disorders, 4(2), 161-166.
Stone, J., Hangge, P., Albadawi, H., Wallace, A., Shamoun, F., Knuttien, M. G., Naidu, S., … Oklu, R. (2017). Deep vein thrombosis: pathogenesis, diagnosis, and medical management. Cardiovascular Diagnosis and Therapy, 7(suppl 3), S276-S284.Vuylsteke, M. E., Colman, R., Thomis, S., Guillaume, G., Degrande, E., & Staelens, I. (2015). The influence of age and gender on venous symptomatology. An epidemiological survey in Belgium and Luxembourg. Phlebology, 31(5), 325-333.
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