Essential Insights On Treating Chronic Venous Stasis Ulcers
- Volume 25 - Issue 7 - July 2012
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What can we do in our practice to help those who are not well insured and are not able to pay out of pocket for treatments that improve outcomes? Are we forced to watch our patients “settle” for what the guideline describes as “substandard care with gauze without compression that pushes them to associated pain, increased infection rates and protracted healing time”?1 For these patients, we can best spend our time by teaching the importance of the basics, such as compression, moist wound healing and elevation. We can also suggest lower priced materials such as Unna boots with cohesive wrap, which patients can change frequently with the aid of a family member.
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.