Chronic venous insufficiency (CVI) and deep venous thrombosis (DVT) are among the most common venous disorders of the lower extremities. By the age of 50, almost 40% of females and 20% of males experience various vein problems, accounting for at least 20 to 25 million Americans (VDF, 2012). CVI and DVT are significant contributors to morbidity and loss of work time worldwide. DVT is a major and potentially preventable cause of mortality. In this paper, these disorders are touched on in detail.

• Epidemiology

CVI affects up to 20% – 40% of adults in the United States (Cleveland Clinic, 2012; VDF, 2012). DVT affects 0.1% of persons per year, but its incidence grows considerably in certain risk groups – elderly, women who take oral contraceptives, pregnant, status post general surgery (Kesieme et al., 2011).

• Pathophysiology

CVI develops when the venous valves do not function properly, and the venous blood refluxes downwards, escaping from its normal path (VDF, 2012). Vein valves fail to support the propagation of blood because the vein walls may be weakened, valves may be absent since birth or trauma, or previous blood clots have damaged the valves. CVI after DVT is called a post-thrombotic syndrome; almost a third of patients develop CVI after DVT (Cleveland Clinic, 2012). Sometimes pelvic obstructions or heart failure induce venous stasis. As a result, gravity pulls the venous blood back down to the ankles. High blood pressure further distends the vein, and varices develop. Tissue metabolism is impaired, so with time, swelling is accompanied by ulcers.

Thrombus develops in the vein valve pocket of the calf, attaches to the vein wall and grows proximally (Kesieme et al., 2011). The thrombus may start intraoperatively or within a couple of days afterward. DVT of the lower limb is classified into proximal (popliteal or thigh veins involved) or distal (calf veins affected). Proximal DVT, which is more fatal, occurs more commonly in cancer patients, heart failure, intubated clients, or those aged above 75 years. Distal DVT is typical for post-operative patients and after immobilization (Huether & McCance, 2012).

• Clinical Presentation

Varices per se carry no problems. However, varicose veins that are associated with CVI cause progressive swelling. Skin changes include discoloration, scarring, eczema and ulceration (VDF, 2012). Aching, tiredness, burning, and muscle cramping occur as the disease progresses. In severe cases, the varicose veins distend and tear, leading to bleeding or thrombose, a condition called superficial phlebitis. DVT typically presents with pains, swelling, tenderness and positive Homans’ sign (Kesieme et al., 2011).

• Patient factors

Typical risk factors for CVI are DVT, obesity, female gender, family history, pregnancy, inactivity, smoking, and age over 50 (Cleveland Clinic, 2012). Virchow triad (endothelial injury, stasis or turbulence, hypercoagulability) was introduced into pathophysiology over a century ago and still proves effective today for thrombosis. 96% of DVT patients have at least one risk factor of the Virchow triad (Kesieme et al., 2011). The risk issues are cancer, immobility, age, previous DVT, and local or systemic inflammation. Sepsis acts as an endothelial damage mechanism. Numerous genetic factors have been identified.

Selected CVI risk factor. Special attention to DVT as a risk factor of CVI must be given here. American Heart Association guidelines on CVI after DVT emphasize that although the pathophysiology of CVI is yet to be studied, restoration of blood flow after thrombosis pharmacologically with anticoagulants restores the normal venous blood flow and reduces the risk of CVI (Kahn et al., 2014). This factor must be always kept in mind when managing a patient with DVT.

Selected DVT risk factor. Long-duration air travel increases the risks of DVT increase the risk by 3% to 12%. The pathophysiology is combined here – stasis, dehydration and hypoxia. Some investigators call DVT after long air travel the ‘economy class syndrome’ (Kesieme et al., 2011).

• Diagnosis

CVI is primarily diagnosed by physical examination, the blood refluxed is visualized by color Doppler scan. The best tool is the duplex exam when the picture of the diseased vein is assessed. Clinical examination is not a reliable way to diagnose DVT (Kesieme et al., 2011). Patients with DVT may be asymptomatic. Clinical prediction rules, like the Wells score, have been developed (Kesieme et al., 2011). DVT verification requires a D-dimer essay to detect thrombi microparticles in the systemic blood circulation, Doppler and duplex scan.

• Treatment

CVI treatment includes avoiding prolonged standing or sitting, the elevation of legs a couple of times daily to reduce swelling, exercise to strengthen the muscle tone and reduce venous reflux, weight control, and skin care. Compression stockings compress the veins under the pressure of 8-10 or 40-50 mmHg, according to the disease stage. Interventions include sclerotherapy or thermal ablation; 10% of patients will require surgical vein ligation, phlebectomy, and stripping (Cleveland Clinic, 2012). DVT treatment aims at thrombus extension and pulmonary embolism prevention. Heparin and low-weight molecular heparin are approved by current guidelines, followed by warfarin for long-term intake (Kesieme et al., 2011). Effective and prompt DVT treatment is the key measure to prevent post-thrombotic CVI (Kahn et al., 2014).

📎 References:

1. Cleveland Clinic. (2012). Chronic venous insufficiency. The Cleveland Clinic. Retrieved from https://my.clevelandclinic.org/health/diseases/16872-chronic-venous-insufficiency-cvi

2. Huether, S.E., & McCance, K.L. (2012). Understanding pathophysiology, 5th Ed. Mosby. ISBN-13: 978-0323078917

3. Kahn, S.R., Comerota, A.J., Cushman, M., Evans, N.S. et al. (2014). The postthrombotic syndr