Vascular Intervention In Difficult Wounds

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Why You Should Get A Vascular Consult For Patients With Arterial Wounds

While vascular surgical intervention is the exception rather than the rule in treating venous ulcers, the opposite is true for arterial wounds. Most intractable wounds due to arterial insufficiency will require correction of the underlying cause of the wound before there is any chance of healing.

This is not to say most patients with arterial insufficiency require surgery. In fact most patients with arterial insufficiency are asymptomatic. Those who are symptomatic usually present with intermittent claudication, which is calf muscle discomfort or fatigue that occurs upon walking a specific distance and resolves with several minutes’ rest. Patients with intermittent claudication are managed medically. Ninety percent will never require surgery.

On the other hand, when arterial insufficiency advances to the stage where intractable arterial wounds develop, surgical correction should be seriously considered.

In regard to podiatric intervention in patients with arterial disease, be aware that it is unfortunately all too common for an arterial wound to occur coincidentally after a minor podiatric procedure, even after you’ve just trimmed the patient’s nails.

When this occurs, many patients understandably connect the two temporally and unfairly blame the podiatrist for the wound. The smart podiatrist will have recognized and documented absent pulses, but the street-smart podiatrist will have sent the patient for comprehensive peripheral vascular evaluation before even touching the patient. In this case, when the wound occurs, the patient will have been prepared. The patient, podiatrist and vascular specialist become a team to manage the problem.

This portrays a typical venous stasis ulcer. Note the location—medial malleolar—and the associated hemosiderosis, dermatitis and brawny edema.
This lateral malleolar wound, although in a less common location, also results from chronic venous insufficiency. Consider possible associated arterial insufficiency particularly when a venous ulcer occurs in an aberrant location.
This is a one-week old bilayered skin prosthesis (Apligraf) overlying and overlapping a venous stasis ulcer.
Prolonged recumbency may have caused this heel pressure ulcer, but underlying arterial disease required correction to allow eventual healing.
Advanced arterial insufficiency accounts for this pattern of diffuse digital gangrene.
Look at this first toe ulcer. It typifies a wound which may have resulted from trauma perhaps compounded with neuropathy, but in which the underlying arterial disease will require work up and management in order to permit wound healing.
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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