Diabetology & Vascular Surgery & Family Medicine
Diabetic foot
The term "diabetic foot" refers to the range of chronic and acute complications affecting the feet of diabetic patients, resulting from the synergistic interaction between three fundamental pathological mechanisms linked to chronic hyperglycemia: diabetic peripheral neuropathy (DPN—damage to the sensory, motor, and autonomic nerve fibers of the lower limbs), peripheral arterial disease (PAD—chronic ischemia due to accelerated atherosclerosis of the distal tibial and peroneal arteries), and increased susceptibility to infections (impaired leukocyte immune response + disrupted skin microbiome + poor vascularization). This is one of the most devastating complications of diabetes in terms of quality of life and social costs: in Canada, diabetes accounts for more than 70% of all non-traumatic lower limb amputations—the vast majority of which (85%) are preceded by a foot ulcer that could have been prevented or treated early. A diabetic patient has a lifetime risk of developing a foot ulcer of 15 to 25%, and the 5-year survival rate after a first major amputation (above the ankle) is less than 50%—worse than that of many cancers. However, studies show that 85% of amputations related to diabetic foot complications are preventable through appropriate therapeutic education, systematic screening for neuropathy and arterial disease, and rapid, multidisciplinary management of lesions. Sensory neuropathy—by eliminating the protective pain that would normally signal an injury or excessive pressure—is the central mechanism explaining why diabetic patients develop ulcers without realizing it: an untreated blister, a shoe that is too tight, or a cut during a pedicure can lead within a few days or weeks to a deep infection, osteomyelitis, and ultimately amputation in a patient whose feet are otherwise pain-free.
Pathophysiology — Neuropathy-Ischemia-Infection Triangle
- Diabetic peripheral neuropathy sensory fiber involvement (loss of touch, heat, and pain sensation → injuries without awareness of danger) + motor fiber involvement (atrophy of intrinsic foot muscles → claw toes + hammer toes → abnormal pressure points on metatarsal heads) + autonomic fiber involvement (anhidrosis → dry skin + hyperkeratosis + fissures → entry points for infections + altered vasomotor control) + neuropathic foot (warm + dry + insensitive + pulses preserved + osteoarticular deformities)
- Diabetic obliterans arteropathy accelerated atherosclerosis predilection for the tibial (anterior + posterior) and peroneal arteries over the femoral artery (unlike non-diabetic PAD) → medial calcification (calcification of the arterial media) → ABI (Ankle-Brachial Index) often falsely normal or elevated despite significant ischemia → need to resort to toe systolic pressure Doppler (TBI - Toe-Brachial Index) or TcPO₂ + cold, pale, livedo-marked ischemic foot + rest pain or claudication
- Diabetic foot infection: impaired phagocytosis and chemotaxis of neutrophils + reduced production of pro-inflammatory cytokines + impaired wound healing + ischemia reduces the delivery of antibiotics and immune cells to the infected site → infections are often polymicrobial (staphylococci + streptococci + enterobacteria + anaerobes + sometimes MRSA in a hospital setting) → rapid spread to deep tissues + fascia + bone (osteomyelitis)
Wagner Classification of Diabetic Foot Lesions
| Wagner Stadium | Lesion description | Recommended support |
|---|---|---|
| Stage 0 | High-risk foot without ulceration + hyperkeratosis + calluses + deformities (claw toes + hallux valgus) + dry skin + fissures + foot at high risk of progression | Proactive prevention + regular podiatric care + therapeutic footwear + education + callus treatment by a podiatrist + monthly or quarterly monitoring based on risk |
| Stage 1 | Superficial ulcer involving skin + superficial subcutaneous tissue + without obvious clinical infection + clean or slightly fibrinous base + well-defined edges | Offloading of the lesion (total contact cast + orthotics + therapeutic shoes) + debridement + appropriate dressings + intensified glycemic control + vascular assessment |
| Stage 2 | Deep ulcer involving tendons, joint capsule, ligaments, and bone without osteomyelitis; local infection often present (erythema, warmth, edema, purulent discharge) | Hospitalization often necessary + appropriate antibiotic therapy (oral or IV depending on severity) + imaging workup (X-ray + MRI if osteomyelitis suspected) + surgical debridement + discharge + urgent vascular assessment |
| Stage 3 | Deep ulcer with osteomyelitis or abscess + deep tissue infection + possible systemic signs | Hospitalization + long-term IV antibiotic therapy (4 to 6 weeks) + surgical debridement + bone resection + urgent vascular evaluation for revascularization if ischemic + high risk of amputation if not revascularized |
| Stage 4 | Localized gangrene (toes + forefoot) + infection + ischemia | Urgent revascularization (angioplasty + bypass) if ischemia + limited amputation + IV antibiotic therapy + emergency vascular surgery + multidisciplinary team |
| Stage 5 | Extensive gangrene of the entire foot + unavoidable major amputation | Transtibial or transtemporal amputation + perioperative care + prosthetic rehabilitation + contralateral foot prevention |
Diabetic Foot Diagnosis and Evaluation
- Foot neurological examination: Semmes-Weinstein monofilament 10g → touch 10 predetermined plantar points → inability to feel the monofilament at ≥ 1 point = significant peripheral neuropathy + 128 Hz tuning fork on the malleolus → early extinction = damage to large myelinated fibers + pinprick test → damage to small fibers + thermal test (hot/cold) + Achilles reflexes (often absent in severe neuropathy)
- Vascular Assessment: Palpation of pulses (posterior tibial + dorsalis pedis) + systolic pressure index (SPI = ankle systolic pressure / brachial systolic pressure) → SPI < 0,9 = AOMI + IPS > 1.3 = mediacalculosis (falsely elevated - do not use alone) + Toe-Brachial Index (TBI - great toe systolic pressure / brachial) → TBI < 0.7 = significant ischemia + TcPO₂ (transcutaneous oxygen pressure) → < 30–40 mmHg = severe ischemia, difficult to heal + arterial Doppler + CT angiogram or MR angiogram if revascularization is considered
- Osteomyelitis diagnosis: probe-to-bone test → insertion of a metal probe into the ulcer → if bone contact is detected = osteomyelitis highly likely (sensitivity 89% % + specificity 85% %) + foot X-ray (bone destruction + osteolysis — a late sign appearing 2 to 4 weeks after onset) + foot MRI = gold standard (sensitivity 90% % + specificity 79% %) → T2 and STIR hypersignal of the affected bone + elevated CRP and ESR + percutaneous bone biopsy for culture (gold standard)
- Classification SINBAD (Site + Ischemia + Neuropathy + Bacterial infection + Area + Depth): Non-healing and amputation risk stratification tool + each variable = 0 or 1 point + total score out of 6 + high score → specialized multidisciplinary team essential
ℹ️
Osteomyelitis of the diabetic foot is the most feared complication—it occurs in 20 to 30% of infected ulcers and is often underdiagnosed. The simplest and most reliable clinical sign is the probe-to-bone test: insert a sterile metal probe into the ulcer—if it reaches the bone (firm, rough contact), the likelihood of osteomyelitis is very high, and an MRI should be ordered immediately. A normal X-ray does not rule out osteomyelitis within the first two weeks.
Treatment
- Intensified glycemic control HbA1c target ≤ 7% (or ≤ 8% in elderly and frail patients) + hyperglycemia → impaired wound healing + immunosuppression + worsening neuropathy → optimizing antidiabetic therapy is a non-negotiable cornerstone of ulcer treatment
- Discharge (off-loading) The most important treatment for healing neuropathic ulcers + Total Contact Cast (TCC) = gold standard → reduces plantar pressure by 80–90% + healing in 90% of cases within 6–12 weeks + alternatives: removable off-loading boots (CROW boot) + custom-made therapeutic shoes + orthopedic insoles + in cases of ischemic lesions: revascularization is a priority before off-loading
- Debridement and local care: Regular (weekly) debridement of necrotic tissue + perilesional calluses + bacterial biofilm → by podiatrist or surgeon + hydrocolloid dressings + hydrofibers + foams + silver (mild infection) + DACC (dialkylcarbamoylchloride dressings) + VAC (vacuum-assisted closure) if large ulcers
- Antibiotic therapy: mild superficial infections (Wagner 1-2 mild) → oral amoxicillin-clavulanate or cephalexin if allergic + moderate to severe infections (Wagner 2-4) → IV piperacillin-tazobactam or ampicillin-sulbactam or carbapenem if ESBL suspected + MRSA coverage if risk factors (vancomycin + linezolid) + variable duration: 1-2 weeks (soft tissue infection) + 4-6 weeks (osteomyelitis)
- Revascularization Percutaneous transluminal angioplasty (PTA) of the tibial arteries + or surgical distal bypass + indicated if TBI < 0.7 + TcPO₂ < 30 mmHg + absence of healing despite optimized treatment + delay < 24–48 h critical ischemia (rest pain + gangrene) → specialized vascular center
- Prevention — Preventive care for the diabetic foot: Daily foot inspection by the patient (use a mirror for the soles) + washing with lukewarm water (DO NOT use a hot basin — impaired temperature receptors → burns) + thorough drying between the toes + moisturizing the heels (10–30% urea cream 1–3 times a week) + trim nails straight across + never cut them too short + wear seamless socks + closed-toe shoes with enough room + never walk barefoot + see a podiatrist every 2 to 3 months
Medical emergency — consult within 24 hours
Any diabetic patient with a foot wound or ulcer showing redness + heat + swelling + pus or odor + or fever must see a doctor within 24 hours — a diabetic foot infection can progress to osteomyelitis and necrotizing fasciitis within days. Call 911 or go to the emergency room immediately if the leg is very red and swollen above the ankle (ascending cellulitis) + if a black or gangrenous area appears + or if the patient is febrile and confused — these signs indicate a severe infection threatening the limb and the patient's life.
For the assessment of diabetic foot at risk, annual screening for neuropathy and PAD, referral to a podiatrist and diabetic foot clinic, and management of early ulcers, Clinique Omicron offers medical consultations at its service points in Quebec and via telemedicine. To make an appointment, visit cliniqueomicron.ca.
Consult at Clinique Omicron
Clinique Omicron's doctors and Nurse Practitioners (NPs) perform the annual diabetic foot exam (monofilament + tuning fork + pulse palpation + NP assessment), classify podiatric risk, optimize anti-diabetic treatment, prescribe podiatry care, refer to the multidisciplinary diabetic foot clinic for ulcers, and coordinate with vascular surgery for revascularization if indicated. Consultations are available at several service points in Quebec and via telemedicine. To book an appointment, visit cliniqueomicron.ca.
The content on this page is provided for informational purposes only and is not a substitute for the advice of a physician, podiatrist, or vascular surgeon. The diabetic foot requires a multidisciplinary approach involving the primary care physician, podiatrist, wound care nurse, vascular surgeon, and diabetologist to optimize healing chances and prevent amputations.
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