School of Podiatric Medicine - Student Research

Document Type

Poster

Publication Date

Winter 12-5-2025

Abstract

Purpose: To evaluate the association between small arterial disease with medial artery calcification (SAD-MAC) and increased risk of osteomyelitis in diabetic foot patients. This study explores how impaired microvascular perfusion contributes to ischemic ulcers, infection progression, and reduced antibiotic efficacy, leading to poor healing and higher amputation rates.

Methods: A retrospective review was conducted on nine diabetic patients with chronic kidney disease, hypertension, and peripheral vascular disease who presented with ischemic or gangrenous toes. Patients lacking radiographs or with non-diabetic ischemic etiologies were excluded. Radiographs were evaluated for small arterial disease with medial artery calcification (SAD-MAC) and graded using the Ferraresi classification (mild = 1-2, moderate-severe = 3-5), where 1 represents isolated focal calcification and 5 indicates multiple arterial segments. Clinical data, wound status, presence of osteomyelitis, and amputation level were documented.

Results: All patients demonstrated radiographic evidence of small arterial disease with medial artery calcification (SAD-MAC), with moderate to severe calcification (scores 3–5). Non-healing ischemic ulcers and digital gangrene were present in every case. Four of nine patients (44%) developed confirmed osteomyelitis based on radiographic and laboratory findings, all of whom required distal amputation. Reported rates of osteomyelitis in diabetic foot ulcers range from 15–30%, suggesting a markedly higher incidence among patients with SAD-MAC in this series. Literature supports that medial artery calcification impairs distal perfusion, limiting leukocyte delivery and antibiotic penetration, which contributes to infection persistence and delayed wound healing. Current evidence also demonstrates no significant difference in outcomes between intravenous and oral antibiotic therapy for diabetic foot osteomyelitis, likely due to poor microvascular perfusion in SAD-MAC patients at ischemic sites. Higher MAC severity correlated with deeper infection and slower healing, underscoring SAD-MAC’s prognostic, and pathogenic significance.

Conclusions: SAD-MAC significantly contributes to ischemia, impaired immune response, and poor antibiotic delivery, increasing the risk of osteomyelitis and amputation in diabetic foot patients. Developing reliable methods to diagnose and treat SAD-MAC may enhance antibiotic efficacy, improve infection outcomes, and support early, targeted limb-salvage strategies in high-risk populations.

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