Current Options In Treating Chronic Venous Ulcers
- Volume 17 - Issue 9 - September 2004
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As foot and ankle surgeons, we are constantly reminded that we are the ultimate champions of diabetic foot care. However, another emerging problem is chronic venous insufficiency (CVI) ulcerations. While it does not have nearly the potential impact of limb loss one may see with complications from the diabetic foot, there is an increasing incidence of CVI with the continued aging of the population.
According to current estimates, CVI affects between 0.1 and 0.3 percent of the total population in the United States. The healthcare industry spends $400 million annually on treating CVI. Unlike the diabetic foot, there is minimal limb mortality with CVI, but very high pain morbidity.
In regard to the development of venous hypertension, pressure on the venous side starts to equalize with the arterial side, obstructing normal blood flow. This pooling of blood can lead to valvular incompetence, allowing blood to be pushed from deep to superficial directions and from superior to inferior directions.
A Closer Look At Venous Inflammation
When it comes to the development of venous inflammation, other hemodynamic events occur when blood slows or reverses from the lower extremity. The calf musculator, which acts as a venous pump, forces a backward blood flow as a hydraulic ram. This reverse pressure pushes molecules and cells into areas where they do not belong. Large monocytes are forced into small venules and large protein molecules (fibrinogen) are subsequently forced out of the vessel wall.
There are two leading theories of what causes inflammation with CVI. “White cell trapping theory” contends that capillaries are present where they do not fit. This stretches the endothelial wall of the vessel, exposing collagen to the monocyte which allows binding and activation to macrophage. The activation macrophage starts the cellular inflammatory response in the blood vessel.
The second theory posits that macromolecules such as fibrinogen are forced from the capillary due to venous hypertension. These large molecules become plentiful around the capillary, causing a “fibrin cuff.” This cuff acts as a barrier to the exchange of oxygen and essential nutrients.
Key Diagnostic Insights
If CVI is allowed to continue, inflammation will develop, resulting in the appearance of physical signs. First, the edema can lead to an inverted bowling pin appearance of the leg. One may also see skin changes of hyperpigmentation, lipodermatosclerosis and induration in the perimalleolar and supramalleolar regions. If these signs are ignored, minor trauma may result in a long-term, painfully debilitating ulceration.
As far as the diagnostic workup goes, always start with a thorough history and physical exam as few wounds will heal if existing comorbidities are not controlled and the etiology of the wound is not identified and treated. When it comes to diagnosing venous stasis ulcerations, one should consider the use of duplex ultrasonography, ankle-brachial index (ABI), venography and culture and sensitivity as well as a biopsy. Duplex ultrasonography has good sensitivity and specificity for valvular incompetence. The ABI should be a part of any wound care workup when arterial flow is in question. Venography is more expensive and more dangerous. One should only reserve this modality for procedures in which a vascular surgeon is involved.
Culture and sensitivity are effective for directing specific antibiotic usage. Obtaining a tissue biopsy is also essential with a CVI workup as many wounds mimic venous ulcerations.