Disorder of the Veins and Arteries
Disorder of the Veins and Arteries
Disorder of the Veins and Arteries
Chronic Venous Insufficiency (CVI) and Deep Vein Thrombosis (DVT) are two prevalent disorders that present with many similarities. Understanding the differences between these two similar but very different disorders can prevent needless misdiagnoses, unnecessary treatments, and complications in the treatment of the disease.The Purpose of this paper is to identify the pathophysiology of Chronic Venous Insufficiency and Deep Vein Thrombosis and their similarities and differences. Also, the patient factor followed will highlight the effects of the female gender on the pathophysiology of these illnesses. Lastly, a constructed mind map will highlight the epidemiology, pathophysiology, clinical manifestations, diagnoses and treatment of Chronic Venous Insufficiency and Deep Vein Thrombosis.
Pathophysiology of Chronic Venous Insufficiency
Chronic Venous Insufficiency (CVI) begins with the development of varicose veins in the deep veins. Varicose Veins are veins in which blood have pooled, and this pooling of blood causes swollen, twisted and tangible veins. Usually, veins are structures that have thin stretchable walls with valves used to prevent backflow and pooling of blood in the veins. Because the veins are structures used to bring blood back to the heart, gravity and valve malfunction over time can cause a varicose vein. When blood pooling occurs, the gravity in the veins causes the surrounding tissue to become swollen. Varicose veins can develop into CVI when there is an inadequate venous return over an extended period. Over the years, venous hypertension, circulatory stasis, and tissue hypoxia caused by sluggish circulation and unmet metabolic needs (waste collection and oxygen delivery) produce an inflammatory reaction in the vessels and tissues. This process induces a fibrosclerotic remodeling of the skin which then causes ulceration. (Huether & McCance, 2017).
Pathophysiology of Deep Vein Thrombosis
Deep Vein Thrombosis (DVT) is caused by three factors (the triad of Virchow): venous stasis, venous injury, and hypercoagulable states. DVT’s begins to form when damage occurs to the inner lining of the vessel wall. This damage initiates the clotting cascade to heal the injured epithelium. As the thrombus grows blood pressure increase and blood flow decreases; Increased pressure in the vein behind the clot may produce edema in the extremity, and persistent venous obstruction can lead to Chronic Venous Insufficiency. Complications of DVT include pulmonary embolism and embolic stroke. (Hammer & McPhee, 2014).
Similarities and Differences between the Disorders
The similarity in the risk factors between these two illnesses includes an increase in age, the female gender, pregnancy, a leg injury, and obesity. Differences in the risk factors are that DVT can be a risk factor for CVI, but CVI cannot cause a DVT. To my understanding, everything that causes DVT can potentially can CVI since DVT is a risk factor for CVI. (Johns Hopkins Medicine, n.d.). The epidemiology is different because CVI can be caused by DVT and other separate entities such as valvular dysfunction and gravity. A DVT is only caused by the triad of Virchow. The signs and symptoms are similar in these two diseases processes because a DVT can become CVI over an extended period. However, at times a DVT can present with redness or discoloration and tenderness in a particular location instead of generalized hyperpigmentation like CVI. (Mayo Clinic, 2017). The diagnostic process of these two illnesses is similar in that they both are both diagnosed using an ultrasound and a venogram. The difference is that for the DVT, diagnostics can also include a computerized tomography (CT), magnetic resonance imaging (MRI), and a D-dimer blood test. (Mayo Clinic, 2017). Treatment similarities include moving around, wearing compression stockings, quitting smoking and exercising. Treatment differences include different medications regimes. Complication similarities include venous stasis ulcers, and complication differences include the pulmonary embolism and embolic strokes that are specific to DVT.
Patient Factors: Gender (Female)
Hormones seem to be the only reason why women are at a higher risk for developing chronic venous insufficiency and DVT than men. Apparently there are many drugs that increase the risk of developing a thrombus, many of which are female hormone and oral contraceptives. (Rosendaal, 2016). The influx, duration, and exit of hormones in a pregnant woman during pregnancy cause this patient population to be more at risk of developing a DVT and CVI. Also, with pregnancy come hypervolemia; the increase of fluid volume in the same fluid space can cause the venous hypertension and place pressure on the valves in the vessels, which can cause CVI overtime if the initial stages of the condition are not treated. Now when diagnosing and treating these disorders in the female population, the only changes that I would have to take would be in the pregnant women population. For expecting mothers recommended diagnoses for a suspected DVT is venous compression ultrasonography and recommended treatment for DVT in pregnant mothers are low molecular weight heparin injections, staying active, and wearing compression stockings. Usually d-dimer blood tests are avoided because during pregnancy, a woman’s serum d-dimer is four to five times higher than normal because of her pregnant state (Dresang, Fontaine , Leeman , King, 2008). As for pregnant women that have chronic venous insufficiency, the diagnosis and treatment would be not different from the rest of the population.
Conclusion
The pathophysiology, similarities and differences of these diseases have been discussed, and the pathology has been considered with the patient factor of female in mind.
References
Dresang L.T., Fontaine P., Leeman L., King V. J. (2008).Venous Thromboembolism During Pregnancy. Am Fam Physician,15;77(12):1709-1716. https://www.aafp.org/afp/2008/0615/p1709.html#sec-5
Hammer, G. G. , & McPhee, S. (2014). Pathophysiology of disease: An introduction to clinical medicine. (7th ed.) New York, NY: McGraw-Hill Education.
Huether, S. E., & McCance, K. L. (2017). Understanding pathophysiology (6th ed.). St. Louis, MO: Mosby.
Johns Hopkins Medicine (n.d.). Chronic Venous Insufficiency. Retrieved from https://www.hopkinsmedicine.org/healthlibrary/conditions/cardiovascular_diseases/chronic_venous_insufficiency
Mayo Clinic (2017). Deep Vein Thrombosis. Retrieved from https://www.mayoclinic.org/diseases-conditions/deep-vein-thrombosis/symptoms-causes/syc-20352557
Rosendaal, F. R. (2016). Causes of venous thrombosis. Thrombosis Journal, 14(Suppl 1), 24. http://doi.org/10.1186/s
