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SAS Journal of Surgery | Volume-12 | Issue-09
Extensive Bilateral Plantar Necrosis in a Patient with Diabetes Despite Preserved Peripheral Pulses and CT Angiography without Obstructive Lesions: A Diagnostic Challenge (Case Report)
El Mehdi El Khadir, Nizar Taoussi, Mehdi Benmoussa, Karima El Houassli, Noureddine Lahlou, Mohamed Zoulati, Tarik Bakkali, Hassan Toufik Chtata
Published: Sept. 22, 2026 |
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Pages: 770-776
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Abstract
Background. Extensive bilateral plantar necrosis is an unusual presentation of diabetes-related foot disease, particularly when peripheral pulses are preserved and imaging shows no significant obstructive peripheral artery disease. Case presentation. A 44-year-old man with poorly controlled type 2 diabetes treated with insulin (HbA1c 10%) was admitted with rapidly progressive bilateral plantar lesions. Initial purpuric and ecchymotic plaques progressed over approximately 15 days to extensive dry necrosis of both soles and several toes. The lower limbs were warm, and the femoral, popliteal, posterior tibial, and dorsalis pedis pulses were palpable and symmetrical. CT angiography of the aortoiliac and lower-limb arteries showed patent aortoiliac, femoropopliteal, tibial, and pedal vessels without abnormalities. On Aug 3, 2026, the patient underwent bilateral plantar necrosectomy with partial toe amputations. After removal of the necrotic tissue, the residual tissue showed macroscopic bleeding. On postoperative day 2, the wounds contained viable red tissue and fibrinous deposits. Intravenous amoxicillin-clavulanate (3 g/day) and ciprofloxacin (500 mg twice daily) were combined with serial debridement every other day. The patient also received 10 sessions of hyperbaric oxygen therapy, five days per week. Discussion. Patency of the major arteries does not exclude disease of the plantar or digital arteries, impaired tissue perfusion, or microcirculatory dysfunction. Histopathological examination in this case showed microthrombotic vasculopathy, with intraluminal fibrin- and erythrocyte-rich thrombi in small vessels, vessel-wall thickening and hyalinization, narrowing or occlusion of some lumina, and ischemic necrotic lesions, without the overt destructive inflammation that would support vasculitis. These findings strengthen the hypothesis that microvascular disease contributed in the setting of severely uncontrolled diabetes, but they do not establish isolated diabetic mi


