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Ulceration of the lower extremities is one of the most frequently encountered dermatologic complications in the surgical arena. Comprising a diverse group of cutaneous diseases with very different pathogeneses and manifestations, lower limb ulcerations can be difficult for clinicians to treat appropriately unless the wounds' etiology is properly identified. In addition to understanding that lower extremity ulcerations are the result of three different etiologies—venous, arterial and neuropathic—clinicians must know which clinical presentations correspond to which specific etiologies to treat the conditions appropriately. Failure to do so may result in devastating consequences, including limb loss.

Venous Ulcers

Venous ulcers are the most common form of leg ulcers and occur as a result of chronic venous insufficiency. In patients with chronic venous insufficiency, the venous system of the lower extremities becomes diseased as a result of one of four pathophysiologic mechanisms:¹

• Dysfunction of valves in the superficial and/or communicating veins because of congenital or acquired incompetence;

• Dysfunction of valves in the deep system because of congenital absence, inherent weakness or thrombotic damage;

• Deep venous outflow obstruction rather than valvular incompetence;

• Muscle dysfunction and calf muscle pump failure from inflammatory conditions of the joints or muscles, fibrosis or neuropathies.

In the diseased condition, failure of the venous system to properly control the return of venous blood to the heart and maintain appropriate venous pressure results in a continuously high pressure within the limbs, leading to stasis. Researchers believe that as a result of stasis, the increased and sustained pressures of the venous system within the leg then are transmitted to the capillary circulation, leading to distension of the capillary walls and leakage of macromolecules such as fibrinogen from within the capillaries into the dermis and subcutaneous tissues of the calf. In the extravascular space, fibrinogen polymerizes to form pericapillary fibrin cuffs.¹ It is suggested that this layer of fibrin forms a pericapillary physical barrier to the diffusion of oxygen and nutrients, resulting in cell death and ulceration.¹

The classic presentation of a venous ulcer resulting from chronic venous insufficiency is an ulceration located in the gaiter area of the lower leg—that is, medially from the instep to above the ankle, most commonly over the medial malleolus where the long saphenous vein is more superficial and has the greatest curvature.^1,2 The ulcerations have borders with irregular margins and are either flat or have a slightly steeped elevation. The ulcer base is often shallow and clean with a yellow, fibrinous bed. On physical examination the lower extremities are warm to the touch, having palpable pulses, with no diminishment or impairment of sensation upon monofilament testing.³

Patient history often notes age older than 60 years; obesity; a history of significant leg injury such as a broken leg, stab or gunshot wound or crushing injury; and employment in which patients experience long hours of standing. Previous varicosities and chronic edema that were followed by pruritic dermatitis are also common. Patients also report and present with signs and symptoms consistent with progressive disease changes, such as reddish-brown hyperpigmentation and purpura caused by extravasation of red blood cells into the dermis, collections of hemosiderin within macrophages, melanin deposition and/or lipodermatosclerosis, which is noted most often in longstanding venous disease in which the skin becomes indurated and fibrotic, resulting in the appearance of an inverted bottle.^1,4

Assessment and diagnosis of venous ulcerations can be made based on clinical presentation and history and physical. Nevertheless, many clinicians turn to noninvasive testing procedures and modalities for assistance. This provides for proper identification of disease etiology and, most importantly, appropriate choice of treatment. Noninvasive tests include measurement of ankle brachial index by Doppler ultrasonography to exclude concomitant arterial disease; continuous-wave Doppler studies to evaluate superficial venous incompetence or obstruction; color duplex ultrasound scanning, the current gold standard, for evaluation of venous anatomy and physiology; and photoplethysmography and air plethysmography to measure the degree of venous reflux and the efficiency of the calf muscle pump system.¹

Treatment of venous ulcers is directed primarily at reversing the effects of venous hypertension but also focuses on reducing edema, alleviating pain, improving lipodermatosclerosis, healing of ulcers and preventing recurrence. This is best accomplished by a combination of therapies, including wound dressings, compression bandages, topical and systemic therapeutic agents and surgical modalities.¹

Initial treatment is with debridement of necrotic tissues to allow for proper granulation and epithelialization of the wound. This is accomplished either surgically or by use of autolytic, chemical and/or mechanical dressings. Pneumatic compression devices, compression stockings and Unna's boots are beneficial in decreasing edema by improving venous hypertension, resulting in faster healing of ulcers and prevention.

Pharmaceutical agents have been found to facilitate the healing process systemically and topically by preventing the fibrinolytic abnormalities that exacerbate this disease condition and by eliminating skin infections.

Additional surgical intervention can increase wound healing: Performing split-thickness skin grafting allows for a more rapid epithelialization and granulation of the wound and can prevent further recurrence of ulcers by ligation or sclerosis of problematic veins.¹

Prognosis with venous ulcers is good. Combination therapy provides a faster healing rate, allowing for recovery of a wound within weeks to months, and provides a means for preventing recurrence of ulcerations.

Arterial Ulcers

Arterial ulcers, commonly referred to as ischemic ulcers, are a result of peripheral arterial occlusive disease. In patients with peripheral arterial occlusive disease, the arterial system of the lower extremities becomes occluded and stenotic due to atherosclerotic plaque formation, with deposition of calcium, thinning of the media, patchy destruction of muscle and elastic fibers, fragmentation of the internal elastic lamina and thrombi composed of platelets and fibrin. Lesions most commonly are located in large and middle-sized arteries such as the femoral and popliteal arteries and can extend into the more distal arteries such as the posterior tibial and peroneal vessels.⁵

Patients with arterial ulcers commonly present with lesions that are located on the lateral or pretibial aspect of the leg, on the dorsum of the foot and/or the toes. Ulcerations are typically round or punched-out with well-demarcated borders. A fibrinous yellow base or a true necrotic eschar with scant or absent granulation tissue commonly is seen. Bone and tendon exposure is not unusual.

Physical examination of the lower extremities reveals decreased or absent pulses distal to the occlusion; bruits just distal to the occlusion site due to increased turbulence; muscle atrophy; hair loss; thickened nails; skin that is cool, smooth, shiny and pale or cyanotic; and an increase of capillary refill of more than four to five seconds.^1,6

Patient history often includes age older than 40 years, a medical history of hypertension, hypercholesterolemia, diabetes mellitus and tobacco abuse, along with a family history of vascular disease.

Classic signs and symptoms include complaints of intermittent claudication—pain, ache, cramp, numbness or sense of fatigue in the muscles that is relieved with rest. Other symptoms include supine nocturnal pain that is relieved by dangling of the affected limb from the bed's edge and/or the presence of a sore on the foot that does not heal. Patients with markedly advanced arterial occlusive disease present with complaints of pain of the affected limb or limbs that occurs at rest.^4,5

Assessment and diagnosis of an arterial ulceration can be made by clinical presentation and accurate evaluation and physical examination. The most common test utilized is the ankle-brachial index (ABI) measured by Doppler ultrasonography, which assesses arterial circulation. A measurement of arterial pressures at the arm and leg are calculated and a ratio is determined.¹ A ratio of less than 0.9 is indicative of arterial disease and requires further testing for proper evaluation.

Patients with an ABI of significance are then evaluated by an invasive radiologic test, an arteriogram, which, with the assistance of an injected contrast medium, can visually reveal the exact location of the occlusion and the severity of the disease.

Treatments of arterial ulcerations are directed at treating the underlying condition of peripheral arterial occlusive disease, and the approach is relative to the severity of the disease.⁷ As with venous ulcerations, medical practice has shown that the use of combination therapy is a more successful approach for patients who are suffering from peripheral arterial occlusive disease and its manifestations. Common to the therapy are systemic pharmaceutical agents, specialized wound dressings, surgical intervention and lifestyle changes.

Pharmaceutical options include antihyperlipidemic agents, aspirin and medications such as pentoxifylline and cilostazol, which are aimed at improving intermittent claudication. Wound dressings, applied in a wet-to-dry method, allow for proper wound healing.³ In patients with an ABI of less than 0.5, surgical intervention is required to bypass the occlusive lesions, revascularize the distal tissues and improve the chances of wound healing. In addition to revascularization, surgical intervention for debridement of wounds, and possible split-thickness skin grafts to increase rate of wound healing, may be performed.⁷

Lifestyle changes are a major contributor to the healing process and prevention of further complications. Patients are encouraged to make lifestyle changes such as refraining from all tobacco use, avoiding foods high in lipids and cholesterol and increasing exercise.

Prognosis is good for patients who seek medical attention as soon as symptoms appear, who follow medical regiments as prescribed and who practice the lifestyle changes required to improve their quality of life. Nonetheless, complications from peripheral arterial occlusive disease can occur, including loss of limbs to gangrene due to severe disease or iatrogenic causes such as improper diagnosis and delay of medical care.

Lizamar Korfhage is a surgical physician assistant at the Back Center at Brevard Orthopaedic and Spine Center in Melbourne, FL.

References

1. Valencia, I., Falabella, A., Kirsner, R., & Eaglstein, W. (2001). Chronic venous insufficiency and venous leg ulceration. Journal of American Academic Dermatology, 44, 401-421.

2. Flye, M. (1997). Venous disorders. In: Sabiston, D., & Lyerly, H., eds. Textbook of surgery: The biological basis of modern surgical practice. 15th ed. Philadelphia: W.B. Saunders.

3. Miller, O., & Phillips, T. (2000). Leg ulcers. Journal of American Academic Dermatology, 43, 91-95.

4. Berger, T. (2000). Skin, hair, and nails. In: Tierney, L., McPhee, S., & Papdakis, M., eds. Current medical diagnosis and treatment. 39th ed. New York: McGraw-Hill Professional Publishing.

5. Creager, M., & Dzau, V. (1998). Vascular disease of the extremities. In: Fauci, A., Braunwald, E., & Isselbacher, K., et al, eds. Harrison's principles of internal medicine. 14th ed. New York: McGraw-Hill Book Co.

6. Hafner, J., Schaad, I., Schneider, E., Seifert, B., Burg, G., & Cassina, P. (2000). Leg ulcers in peripheral arterial disease (arterial leg ulcers): Impaired wound healing above the threshold of chronic critical limb ischemia. Journal of American Academic Dermatology, 43, 1001-1008.

7. Newman, A. (2000). Peripheral arterial disease: Insights from population studies of older adults. J Am Geriatr Soc., 48, 1157-1162.