Skip to main content

Advertisement

ADVERTISEMENT

Case Report

Martorell’s Ulcer Revisited

Introduction In the 1940s, Martorell[1] described a unique, ischemic ulcer of the leg as a complication of hypertension. Hines and Farber[2] subsequently confirmed the existence of this ulcer and reported 11 cases of Martorell’s ulcers. The classic presentation of this ulcer includes a superficial ulcer on the lower extremity, poorly controlled or long-standing diastolic arterial hypertension in both the extremities, bilateral symmetry that may manifest as a pigmented lesion on the contralateral leg, a history of minimal trauma, which may not be remembered, and moderate to severe pain often out of proportion to the size of the ulcer.[3] The lesion is more common in female patients than in male patients, rarely seen in African Americans, and is most often seen in women between the ages of 55 and 65.[4] These lesions are refractory to local wound care or more aggressive therapy and may progress by irregular extension of the ischemic area. The diagnosis also requires that other causes of lower-extremity ulcers, such as arterial insufficiency, venous insufficiency, and systemic disease, be excluded.[5] These lesions also have a characteristic appearance on biopsy according to Hines and Farber. There is arteriolar stenosis, hyalinization between the endothelium and the elastica interna, and an increase in the size and number of nuclei indicating endarterial proliferation. Here the authors describe a case that is classic in presentation, pathology, and management. Although rare, this disease is important to understand in order to hasten diagnosis and treatment and, thereby, reduce the time of disability for the patient. Case Report A 59-year-old Caucasian woman presented with a five-centimeter-diameter superficial ulcer on the anterolateral aspect of her left leg. The patient stated the ulcer had developed after minimal trauma (Figure 1). The wound failed to respond to extensive antibiotic therapy, local wound care, and application of local tissue growth factors by her previous physician. The patient denied a history of diabetes or peripheral vascular disease. On physical exam, the patient had significant hypertension with a diastolic blood pressure greater than 120mmHg despite antihypertensive therapy with a calcium channel blocker. The anterolateral supramalleolar region of the contralateral leg had a healed ulcer that had been covered with a skin graft three years earlier. There were no signs of venous stasis, such as edema or brawny induration. The patient had palpable pedal pulses and a normal ankle/brachial index (ABI). The patient was a smoker, and Beurger’s disease was considered. The patient ceased all use of tobacco while being treated, but this did not lead to resolution of the ulcer. The ulcer was treated with debridement, elevation, and wet-to-dry saline dressings. The wound continued to progress. Factitious injury was eliminated with occlusive dressing while a negative hematologic and rheumatologic workup was completed. The wound had progressed with peroneus brevis and peroneus longus tendon exposure. Arteriogram did not indicate any significant arterial insufficiency. Attempted radial forearm free flap coverage of the 8cm x 7cm ulceration failed at post-operative Day 6 from venous stasis secondary to an extended period of dependency. The ulcer was progressive, particularly at the margins where tissue may have been traumatized during operation. Telltale satellite lesions developed (Figure 2). A biopsy of the ulcer exhibited hyalinization and thickening of the arteriole media (Figure 3). Quantitative and qualitative wound cultures exhibited superficial colonization with no deep infection. A Martorell’s ulcer was suspected at this time, and aggressive antihypertensive therapy with clonidine, an ACE inhibitor, and a beta-blocker was initiated. The patient’s diastolic blood pressure stabilized to

Advertisement

Advertisement

Advertisement