Essential Insights On Treating Chronic Venous Stasis Ulcers
What can we do to address prevention, psychosocial issues, recurrence prevention and treatment? Although more clinical evidence is necessary, recent work by Finlayson and colleagues suggests that psychosocial factors of low levels of social support and self-efficacy are “significantly associated with a greater risk of recurring venous leg ulcers.”3 Accordingly, we should encourage the engagement of friends, family and other sources of support.
Essential Diagnostic Considerations
According to the Clinical, Etiology, Anatomy, Pathophysiologic (CEAP) Classification, a venous type ulcer is one of six different types (see “A Pertinent Overview Of The CEAP Classification” at left).8
Category 1 shows telangiectasias or reticular veins like spider veins.
Category 2 will show varicose veins.
Category 3 will start showing varicose veins along with leg swelling.
Category 4 will show evidence of venous stasis skin changes.
Category 5 reflects skin changes in conjunction with healed ulcerations.
Category 6 describes skin changes in association with active ulceration.
Patients in categories 5 and 6 will most likely need wound care management whereas those in categories 1 to 4 will require long-term preventive treatment. Note that if chronic venous insufficiency goes untreated, it might result in secondary lymphedema, which may further complicate venous ulcer management.
The revised CEAP classification of chronic venous disease defines a venous ulcer as a full thickness defect of skin, most frequently in the ankle region (usually in the gaiter region), which fails to heal spontaneously and is sustained by chronic venous disease.8
The exact etiology of venous ulceration is unknown. However, the mechanism of venous ulcers is theoretically due to the incompetence of the valves causing intraluminal pressures to increase. When venous hypertension is present, blood does not pump as effectively in or out of the area and pools accordingly. Venous hypertension may also stretch veins and allow blood proteins to leak into the extravascular space, isolating extracellular matrix molecules and growth factors, and preventing them from helping to heal the wound.9 Leakage of fibrinogen from veins as well as deficiencies in fibrinolysis may also cause fibrin to build up around the vessels, preventing oxygen and nutrients from reaching cells.9 This improper functioning of vein pressure results in transudation of inflammatory mediators into the subcutaneous tissues of the lower extremity and subsequent breakdown of the tissue including the skin.
Symptoms may include mild to severe edema of leg as well as sensations of fatigue and heaviness with burning or itching. It is helpful to let patients know that sufficient reduction of edema can offer partial relief, if not full relief, of the aforementioned symptoms. There may also be a rash, redness, brown discoloration of hemosiderin staining, lipodermatosclerotic changes as well as xerosis with thick hyperkeratotic plaques. These shallow lesions occur on the medial lower extremity just above the ankle where venous pressure is greatest due to the presence of large communicating veins.