Successful Pharmacologic Treatment of Lower Extremity Ulcerations in 5 Patients With Chronic Critical Limb Ischemia

Steven M. Dean, DO, Patrick S. Vaccaro, MD

Disclosures

J Am Board Fam Med. 2002;15(1) 

In This Article

Case 1

An 84-year-old minimally ambulatory man with a history of type 2 diabetes mellitus, hypertension, hyperlipidemia, coronary artery disease, and previous tobacco use (1 pack per day for 5 years) was referred to the office for evaluation of a nonhealing, painful ulceration on the right distal hallux. The pain in his great toe worsened at night and was relieved by placing the extremity in a dependent position. The ulcer had been present for approximately 14 weeks and had failed to improve despite various medications, including topical mupirocin, aspirin, and a 2-month course of antibiotics (which included 4 weeks of parenteral antibiotics).

When examined, his feet were cool bilaterally with dependent rubor and pallor on elevation. A distal ulceration was observed on the right hallux, the base of which was composed primarily of dry brin and necrotic debris. There was only a minimal amount of granulation tissue (Figure 1A). The underlying bone was not exposed or palpable. The femoral and popliteal pulses were normal, but the dorsalis pedis and posterior tibial pulses were absent.

(Case 1). A. Ischemic right hallux ulceration. B. Right hallux after 10 weeks of therapy with cilostazol. The ulcer had healed with visible evidence of reepitheliazation.

The patient's right ankle-brachial index measured 0.52, and his ankle systolic pressure was 64 mm Hg. The ankle-brachial index was falsely elevated because of partially calcified vessels. Arterial Doppler ultrasonography displayed posterior tibial and dorsalis pedis monophasic waveforms. In addition, the pulsed volume recording waveform at the right ankle was severely dampened (approximately 5-6 mm of amplitude) indicating severe large-vessel ischemia. The transmetatarsal waveform was at, and the hallux waveform showed erratic, minimal pulsatility (suggesting a motion artifact, not true perfusion), which was indicative of concurrent severe small-vessel ischemia (Figure 2A). The distal plethysmographic waveforms were obtained after 5 minutes of external warming to eliminate possible vasospasm.

(Case 1). A. Pretreatment noninvasive arterial study. Right ankle-brachial index measured 0.52, with an ankle systolic pressure of 64 mm Hg. Severely dampened right ankle pulsed volume recording waveform indicates severe ischemia and suggests an ankle-brachial index falsely elevated because of arterial calcification. The right transmetatarsal waveform is flat, and hallux waveform displays erratic, minimal pulsatility (suggesting motion artifact, not true perfusion), indicating concurrent severe small-vessel ischemia. B. Posttreatment noninvasive arterial study. Right ankle-brachial index increased to 0.57 (ankle systolic pressure increased to 82 mm Hg). Right pulsed volume recording waveforms at level of ankle, transmetatarsal, and hallux displayed increased pulsatility (note the increased amplitude of ankle waveform to 7-8 mm)

Percutaneous or surgical intervention was not considered an ideal treatment option for this patient because of his limited ambulatory status, advanced age, and comorbid disease. As a result, he was prescribed cilostazol, 50 mg twice a day (dose adjusted to accommodate concurrent nifedipine therapy). After 10 weeks of cilostazol therapy, the ulcer had healed (Figure 1B), and the patient's ischemic pain had resolved. A follow-up pulsed volume recording examination displayed subtle increased pulsatility within the ankle waveform (amplitude increased to 7-8 mm) and new pulsatility at the transmetatarsal and hallux levels (Figure 2B). The ankle-brachial index increased from 0.52 to 0.57 (ankle systolic pressure increased from 64 to 82 mm Hg).

The patient returned 3 months after the follow-up visit for evaluation and treatment of a recurrent right hallux ulceration. He had mistakenly discontinued cilostazol a month earlier and subsequently traumatized the right distal hallux, provoking a second, stereotypical ischemic ulcer. Cilostazol was again prescribed, and the patient was counseled about the importance of adhering to therapy. The second ulcer healed within 2 months. By the 1-year follow-up visit, the patient was continuing to take cilostazol faithfully and has remained free of ulcers.

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