How To Manage Venous Stasis Ulcers

By Tamara D. Fishman, DPM

Given the poor healing rates, high recurrence and castly nature of venous stasis ulcerations, this author offers a primer on key clinical signs, helpful insights on compression and wound care modalities, and underscores the importance of appropriate referrals. In the United States, venous stasis ulcers have been estimated to cause the loss of 2 million working days and reportedly incur treatment costs of approximately $3 billion per year.1 The likelihood of developing venous stasis ulcerations increases with age. It is well known that patients with a history of venous insufficiency are more likely to develop venous ulcerations. Paraplegic patients are also more likely to develop venous ulcerations due to the fact that the calf muscle is immobile.    Lower extremity venous ulcers have a variety of etiologies. However, chronic venous insufficiency (CVI) is the most common cause of lower extremity venous ulcers. Ulcer healing rates can be poor with up to 50 percent of venous ulcers open and unhealed for nine months or longer. Venous ulcer recurrence rates are also troubling with up to one-third of treated patients experiencing four or more episodes of recurrence.    Chronic venous insufficiency is an advanced stage of venous disease caused by either superficial or deep venous pathology. Patients with CVI have an impaired venous return, which usually occurs over the course of multiple years and is caused by reflux, obstruction or calf muscle pump failure. This all leads to sustained venous hypertension and ultimately to various clinical complications such as edema, eczema, ulceration and lipodermatosclerosis. Chronic venous insufficiency results from dysfunctional valves that decrease venous return and subsequently increase venous pressure.

A Guide To Identifying Key Clinical Signs

The high venous pressure results in the presence of edema as well as the extravasation of red blood cells and large protein molecules that leak out from capillaries. Initially, clinicians will note a soft pitting edema but the skin becomes thickened over a long period of time. The venous hypertension also produces a fibrin cuff around capillaries. The fibrin cuff then inhibits oxygen diffusion to adjacent tissues, leading to local tissue atrophy and, eventually, skin ulceration. These clinical signs are often referred to as lipodermatosclerosis or postthrombotic syndrome.    Podiatrists will most commonly locate venous stasis ulcerations on the medial or lateral aspects of the lower extremities. Characteristically, these ulcers have an irregular shape with well-defined margins. They present with edema, hyperpigmentation — due to the breakdown of the red blood cells and the deposition of hemosiderin and melanin — and skin induration (fibrosed skin). These patients may present with stasis dermatitis, erythema, fissuring, dryness, scaling of the skin and brown skin discoloration.    When patients present with venous stasis ulcers, DPMs should also evaluate for signs and symptoms of any underlying systemic issues, such as congestive heart failure, hypoalbuminemia, malnutrition, diabetes and arterial insufficiency, and make appropriate referrals if warranted.


Great the point, concise. Thanks, JGF PA-C

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