Chronic Venous Insufficiency and Deep Vein Thrombosis
Chronic Venous Insufficiency and Deep Vein Thrombosis
Several different vein and artery disorders may share a lot of common symptoms. For example, both chronic venous insufficiency (CVI) and deep vein thrombosis (DVT) have similar symptoms, but there are some differences in their pathophysiological processes and various non-invasive diagnostic methods exist that can be used to help physicians distinguish between these two conditions. An examination of various risk factors showed that previous trauma has a high correlation with those disorders while gender is not a significant risk factor. CVI is more prevalent in women than men, and studies on the prevalence of DVT between genders show mixed results. In both cases, gender does not significantly interfere with the diagnosis or treatment of both conditions.
CVI occurs when the veins are unable to pump enough blood back to the heart. Several malfunction in the venous mechanisms, including valvular malfunctions in deep or superficial veins, perforator valve malfunction, obstruction, muscle pump dysfunction, changes in hemodynamics of veins, and a combination of more factors, can cause CVI. CVI often follows DVT because the valves suffer damage during DVT and are unable to perform.
DVT usually develops in the calf region and expands towards the heart. The femoral, popliteal, and iliofemoral vein are often affected in the beginning stages, but DVT cases that progress can often affect the iliac vein or the inferior vena cava. The main difference in the physiology between CVI and DVT is the type of veins they affect and the mechanisms they affect. In DVT, deep veins are affected and clots are formed while CVI mainly affects superficial veins and prevents blood from flowing back to the heart.
Although DVT is similar to arterial thrombosis, there is a key difference. Arterial thrombosis occurs when blood clots occur in arteries, but the walls of the vessels needs to be damaged for coagulation to occur within arteries (López & Chen, 2009). There is no such requirement for DVT. Also, platelets can cause clots in veins, but they are more common in clots caused by arterial thrombosis (López & Chen, 2009). Finally, the cause of those conditions is often different. Arterial thrombosis is often caused by atrial fibrillation. DVT can be caused by hemiparesis from stroke or occur without clinical causes in 25 percent of cases (Ho, 2010).
While gender is possibly correlated with DVT and CVI, it is only a secondary risk factor because some studies identified it as a weak risk factor or because it varies in prevalence across geographical locations. For example, Kröger et al. (2004) found that gender is only a minor risk factor for developing DVT while Cogo et al. (1994) found that male gender is a secondary factor associated with acute DVT. Ho (2010) does not include gender as a clinical risk factor for DVT, but claims pregnancy is a moderate risk factor, so it is possible to suggest that DVT may be prevalent among the female gender.
Because the literature often provides contradictory evidence on the topic, it is not possible to make a conclusion on the correlation between gender and DVT. CVI prevalence varies by geographical locations, but female gender turned out to be one of the established risk factors as it is mainly prevalent among women (Beebe-Dimmer, 2005). Therefore, while it is possible to make initial assumptions based on gender, it is not possible to make a solid diagnosis for both conditions using gender.
The diagnosis of both conditions is possible with venous duplex imaging (Eberhardt & Raffetto, 2005). However, it is important to conduct various assessments to eliminate other conditions that may share similar symptoms and gain more evidence to support the diagnosis and initiate the correct treatment. It is also important to eliminate certain tests when they may prove inconclusive or result in a wrong diagnosis.
I would start the diagnosis for both conditions with a physical examination because it can be used to detect various CVI symptoms. By using palpitation and skin examination with a tourniquet test, it would be possible to plan out the further course of treatment once the diagnosis is complete (Eberhardt & Raffetto, 2005). However, the physical examination itself would be useless because many conditions may mimic DVT or CVI (Ho, 2010), so further diagnosis would be conducted with non-invasive methods.
Photoplethysmography would be used if the initial examinations show a possibility that the patient suffers from CVI. Venous duplex imaging can be used in both cases because it is an established method for diagnosing DVT, but studies also showed that it can be used to eliminate DVT and diagnose CVI (Eberhardt & Raffetto, 2005). Gender plays a role in diagnosing DVT when the patients are pregnant women. When using compression ultrasonography, the initial test on pregnant women may be negative, so repeating the scanning after five or seven days is necessary for obtaining accurate results (Ho, 2010).
When treating DVT, gender does not play a significant role. All patients require administration of anticoagulant medicine within 24 hours to prevent complications (Weinmann & Salzman, 1994). Further treatment would include antithrombotic or antiplatelet drugs, and planning the treatment and surveillance would be planned in compliance with the patient’s age rather than gender because it is a significant risk factor for DVT-related complications (Weinmann & Salzman, 1994).
Treating CVI would depend mainly on the patients’ medical history and the stage of the disorder. For example, pressure therapy, skin care, and physical activity are required and recommended in early stages. In later stages of CVI or severe forms, various interventions and surgery are required, but they all have certain limitations. For example, surgery, such as valve reconstruction, would be possible only in situations when DVT was not a previous condition because of possible complications that could occur after internal bleeding problems (Eberhardt & Raffetto, 2005). The choice of the intervention would be based on existing symptoms and the expected trajectory of disorder development.
Beebe-Dimmer, J. L., Pfeifer, J. R., Engle, J. S., & Schottenfeld, D. (2005). The epidemiology of chronic venous insufficiency and varicose veins. Annals of Epidemiology, 15(3), 175-184.
Cogo, A., Bernardi, E., Prandoni, P., Girolami, B., Noventa, F., Simioni, P., & Girolami, A. (1994). Acquired risk factors for deep-vein thrombosis in symptomatic outpatients. Archives of Internal Medicine, 154(2), 164-168.
Eberhardt, R. T., & Raffetto, J. D. (2005). Chronic venous insufficiency. Circulation, 111(18), 2398-2409.
Ho, W. K. (2010). Deep vein thrombosis: Risks and diagnosis. Australian Family Physician, 39(7), 468-474.
Kröger, K., Weiland, D., Ose, C., Neumann, N., Weiss, S., Hirsch, C., & Scheulen, M. E. (2006). Risk factors for venous thromboembolic events in cancer patients. Annals of Oncology, 17(2), 297-303.
López, J. A., & Chen, J. (2009). Pathophysiology of venous thrombosis. Thrombosis Research, 123, S30-S34.
Weinmann, E. E., & Salzman, E. W. (1994). Deep-vein thrombosis. New England Journal of Medicine, 331(24), 1630-1641.