How To Manage Venous Stasis Ulcers

Author(s): 
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.

Critical Keys To Look For In The Diagnostic Workup

In regard to the treatment of venous stasis ulcerations, one must address the underlying cause, which is venous insufficiency. The etiology may include incompetent superficial veins and perforators as well as postphlebitic syndrome. These factors will result in persistent venous hypertension and a rise in capillary pressures with the leaking of fibrinogen into the tissues.    In order to prevent venous ulcerations, patients should wear compression stockings. These stockings compress the veins and facilitate adequate blood flow, making it more difficult for blood clots to form and swelling to occur. Compression therapy is the cornerstone of nonoperative management of venous stasis ulcers. Compression therapy may include compression wrappings and custom stockings.    However, as a precursor to compression therapy, one must assess arterial flow with the ankle-brachial index (ABI). Many medical professionals have suggested that an ABI below 0.8 to 0.7 is a contraindication for compression therapy. If patients complain of increased pain with venous ulcers, clinicians should have a higher index of suspicion for arterial insufficiency. Ruling out arterial insufficiency is important as the application of compression to diseased arteries can cause additional damage to the ulcer and lead to further complications in the healing process. Other contraindications for compression therapy include phlebitis and suspected deep venous thrombosis (DVT).    Prior to managing venous stasis ulcers, the clinician must also rule out an ischemic component to the etiology. Additionally, one may consider a biopsy to eliminate vasculitis as the etiology of the ulcer. If the wound presents with surrounding cellulitis, one should administer systemic antibiotics.

Facilitating Successful Outcomes With Compression

Prior to applying any compression system, one should thoroughly cleanse the ulcer and apply a non-adherent dressing to the ulcer. Depending on the characteristics of the venous ulcer, the healthcare provider may select another type of wound management material.    The type of dressing clearly depends upon the wound characteristics at the time of the dressing change. Venous ulcers are usually highly exudative throughout the course of the healing process. Venous ulcers typically appear with a yellow fibrinous material that covers the wound but clinicians should differentiate this from true exudate. One must measure the ankle circumference and then choose the appropriate compression system.    The first layer of dressing consists of a soft wool bandage to protect any bony prominences around the ankle and shin area. One would then apply a crepe bandage as the second layer of dressing. The third layer of dressing is an elastic bandage that will serve to apply the compression. The fourth and final layer will apply even more compression and serve to keep all the bandages in place. One can leave this bandage system in place for up to seven days but the clinician may change the dressing if fluid is leaking. The treating physician must evaluate the length of time that the compression system is left in place. The system described here is referred to as a four-layer compression bandage system.

A Closer Look At Appropriate Wound Care Modalities

Medical treatment of venous stasis ulcerations is dependent on the operative management and repair of the underlying cause for venous insufficiency (see “What You Should Know About Procedures For Vascular Insufficiency” below). However, for many patients, surgery is not a practical or viable option. Therefore, clinicians must manage these wounds without surgery.    In addition to facilitating edema reduction in the lower extremity via appropriate compression, podiatric physicians must use appropriate wound care products as well.    Vacuum Assisted Closure therapy (VAC, KCI). Vacuum assisted closure therapy is a therapeutic product for the management of acute, subacute and chronic wounds. Vacuum assisted closure involves placing an open-cell foam dressing into the wound cavity and applying controlled subatmospheric pressure, typically 125 mmHg below ambient pressure. The therapeutic objectives of VAC therapy are removing chronic edema, increasing local blood flow and removing infectious material/fluid in order to enhance the formation of granulation tissue.    Applying negative pressure to the wound bed creates tension among adjacent cells, which reportedly alters the shape of the cells. This subsequently stimulates cell growth and division, drawing the edges of the wound to the center and eventually facilitating wound closure. The contraindications for this treatment option include necrotic tissue, untreated osteomyelitis, malignancy in the wound and fistulas to organs or body cavities.    Overall, VAC therapy enhances the body’s natural capability to heal by accelerating the formation of granulation tissue. It improves perfusion through the removal of edema and decreases the bacterial colonization in the wound.    Apligraf (Organogenesis). Apligraf is a bilayered, bioengineered cell therapy indicated for the treatment of venous ulcers. Apligraf is indicated for use with standard therapeutic compression in the treatment of uninfected partial- and or full-thickness skin ulcers due to venous insufficiency of greater than one month’s duration that have not adequately responded to conservative wound care modalities.    Apligraf is contraindicated for use on clinically infected wounds and in patients who have known allergies to bovine collagen or hypersensitivity to the components of the shipping medium.    Acticoat (Smith and Nephew). Acticoat is a treatment option in the management of venous stasis ulcers. The use of silver has been used to fight infections since the late 19th century. Silver kills microbes by poisoning respiratory enzymes and components of the microbial electron transport system as well as impairing some DNA functions.    Acticoat is comprised of a rayon/polyester core that helps manage moisture and controls the release of silver-coated, high-density polyethylene mesh that facilitates the passage of silver through the dressing. For highly exudating wounds, one should apply the Acticoat dry. The exudate will cause the release of the dressing’s silver ions into the wound bed. If the wound is not exudating, then the clinician must moisten the dressing with sterile water. Acticoat is not helpful in healing non-infected wounds or wounds that present with eschar.    Arglaes (Medline). Arglaes is a film dressing that provides a continuous and controlled release of silver ions. It reportedly maintains an antimicrobial barrier for up to seven days, continuously releasing the silver ions through the use of controlled release polymers. Given the emergence of resistant organisms, clinicians may want to consider Arglaes as it appears to control the bacteria in wounds and prevent bacterial contamination. Arglaes also provides a moist environment to facilitate the healing process and is suitable for many wound types. Arglaes is not helpful in healing non-infected wounds or wounds that present with eschar.

In Conclusion

Venous stasis ulcers are the result of prolonged venous insufficiency and hypertension of the lower extremities. Typically, clinicians will locate venous stasis ulcers just proximal to the medial malleolus but they may sometimes appear proximal to the lateral malleolus and, in rare instances, at other locations.    Despite intensive treatment, there will be some patients who have intractable ulcers that will just not heal. In these cases, the goal of treatment is to keep these ulcers under control and reduce the effects on the patient’s day-to-day life activities. Failure to identify and treat the underlying venous hypertension is a common reason for failed healing or reoccurrence of these types of lower extremity ulcers. Dr. Fishman is the Chairman of the Wound Care Institute in North Miami Beach, Fla.
 

 

References:

References 1.     Bergan JJ, et al. Chronic venous disease. N Engl J Med 2006; 355 488-98. 2.     Burnard KG, Browse NL. The cause of venous ulcerations. Lancet 1982; 31:243. 3.     Lopez A, Phillps T. Venous ulcers. Wounds. 1998; 10:149-157. 4.    Thomas Hess C. Management of the patients with venous ulcer. Advances in Wound and Skin Care 2000.; 13:79-83. 5.     Compression therapy for venous leg ulcers. Drug and Therapeutics Bulletin April 2000.

 

Comments

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

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