Vascular Intervention In Difficult Wounds

Author(s): 
By Richard M. Stillman, MD, FACS

About four of 1,000 people will develop a leg ulcer during their lives, but the prevalence of leg ulcers rises dramatically with age, increasing to about 1 percent in people over the age of 60 and 2 percent in people over the age of 80. In the U.S., about 3 million people suffer from leg ulceration, costing an annual $4 billion in treatment costs and losses of over 2 million days from work.
In general, diagnosing the cause of leg and foot wounds requires examining the wound, the extremity and the patient. Let’s start by taking a look at venous problems.
Any disease state that leads to venous insufficiency or venous hypertension can lead to venous stasis disease. Such pathologies include varicose veins, deep venous thrombosis and congestive heart failure. The common denominator of these divergent conditions is that venous valves become incompetent.
Primary venous valvular incompetence manifests as the gradual onset of superficial varicosities. Venous ulcers are three times more common in women than men because varicosities, the most common cause of venous insufficiency, are that much more common in females. Interestingly, because the left iliac vein is somewhat more prone to develop venous valvular incompetence than the right iliac vein, varicosities are about 10 percent more common in the left lower extremity. In the case of deep vein thrombosis, valvular incompetence results from valve damage during the acute thrombotic phase. As the thrombus recannalizes, the now incompetent valves become exposed.
In the case of congestive heart failure, elevated pressures on the right side of the heart are transmitted to the iliac veins and distend these veins to the point that the valve leaflets fail to coapt and hence become functionally incompetent. With incompetence of the proximal valves comes a cascade effect to cause distension and incompetence of more and more distal valves. When venous valves become incompetent, venous blood flow becomes bidirectional, causing venous hypertension in the distal leg and foot.
Venous hypertension enlarges the capillary bed in the skin, increases permeability of the capillary wall and allows large molecules such as fibrinogen to extrude. Fibrinogen forms a fibrin cuff around the capillary bed and interferes with oxygen diffusion. Thus, an area of skin becomes relatively ischemic and ulceration-prone. At the same time, leukocytes become trapped in the capillaries, discharging proteolytic enzymes and free radicals that cause tissue necrosis.

How Do You Know An Ulcer Is Due To Venous Disease?
The usual clinical findings in venous stasis ulceration follow from this pathophysiology. First, as I noted above, these ulcers often occur in patients with a history of one of these inciting factors—prior deep vein thrombosis (which may have occurred decades prior), varicose veins or chronic congestive heart failure.

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