1. MULTIMODALITY MANAGEMENT OF DIABETIC FOOT WOUNDS Martin R. Back, MD Associate Professor of Surgery Tampa, FL

2. WHY A WOUND WON’T HEAL 1.ISCHEMIA - PAD, Buerger’s, Raynaud’s, other 2.EDEMA - Venous insufficiency, lymphedema, cardiac/hepatic/renal failure 3.PRESSURE-RELATED - neuropathy, debility/nonambulatory 4.INFECTION 5.FOREIGN BODY 6.MALNUTRITION 7.COMPROMISED IMMUNE FUNCTION - cancer

4. DIABETES DEMOGRAPHICS

7. DIABETIC ATHEROSCLEROSIS Comparison ischemic amputated limbs in diabetics and nondiabetics - Ferrier, 1967 No difference incidence occlusive dz popliteal, tibial, pedal arteries More occlusive dz and calcification of metatarsal and digital arteries in diabetics

8. ABI < 0.6 less chance of healing

9. Toe P < 60 mmHg : less chance of healing

10. DIABETIC ATHEROSCLEROSIS Popliteal / tibial dz - ‘meltdown’ Severe calcific vessels Distal tibial / pedal targets Autologous vein graft bypass over endovascular therapies for multilevel/long-length occlusions Patency equivalent to non-diabetics

11. OPTIMAL DISTAL REVASCULARIZATION : FEMOROTIBIAL BYPASS WITH SAPHENOUS VEIN GRAFT CONTRAINDICATIONS - advanced / necrotizing foot infections, advanced gangrene in chronic renal failure patients

13. DIABETIC PERIPHERAL NEUROPATHY Symmetric mixed polyneuropathy increased incidence with duration of DM majority pts after 10-15 yrs affects distal lower limbs segmental demyelination etiology of injury ? ischemia metabolic (polyol, prostaglandin, carnitine, GF) immune

14. DIABETIC PERIPHERAL NEUROPATHY MANIFESTATIONS Sensory loss early dysesthesias and painful paresthesias loss of vibratory sense loss of light touch and pain “stocking & glove” distribution loss of deep tendon reflexes Motor loss atrophy foot intrinsic musculature pes cavus deformity, hammer toe formation prominent MT heads, migration MT fat pads arch collapse ===> Charcot’s arthropathy

15. DIABETIC PERIPHERAL NEUROPATHY Autonomic loss sympathetic (earlier) & parasympathetic loss foot anhidrosis vasomotor dysfunction (AV shunting, orthostatic hypotension) GI, GU dysfunction increased mortality (cardiac, renal)

16. IMPLICATIONS OF NEUROPATHY & ‘ARCHITECTURAL’ FOOT CHANGES

17. COMPLICATIONS OF ‘END- STAGE’ NEUROPATHY & CHARCOT FOOT ANATOMY

19. TREATMENT NON-INFLAMMED NEUROPATHIC ULCERS No role for antibiotics Off - loading orthopedic cast shoes, heel ‘cutoff’ sole, crutches total contact cast minimal ambulation / bedrest Wound cleansing & dressing changes Debridement / Metatarsal head resection Topical recombinant human PDGF, other agents Gabapentin/neurontin for dysethetic symptoms/pain

21. PRIOR MULTI-DIGIT AMPUTATIONS WITH RECURRENT PLANTAR NEUROPATHIC ULCER - transdorsal distal metatarsal / head resection

22. TREATMENT GOALS : Control local sepsis (operative) Control systemic sepsis (antibx) Revascularization for foot salvage Staged wound closure / skin coverage

23. TREATMENT NON - LIMB THREATENING INFECTIONS 1 - 2 week course oral antibiotics ? value topical antibiotics Non-invasive vascular evaluation Treatment neuropathic ulcer Frequent, careful follow-up

24. The Septic Diabetic Foot ‘a little painful’ per patient, first visit for med care chronic plantar ulcer not recognized / treated worsening hyperglycemia marked leukocytosis extensive cellulitis medial ankle, malodorous wound weak monophasic pedal Doppler, palpable femoral pulse

25. DIABETIC FOOT INFECTION Broad-spectrum IV antibx Aggressive volume replacement (saline) Glycemic control (IV insulin) Cardiac protection, anti-platelet Probable plantar space abscess / near- necrotizing infection = unsalvagable Urgent explore/debride  ankle disarticulation  staged BKA

26. NON-HEALING TMA TREATED WITH PROLONGED VAC SPONGE THERAPY

27. DIABETIC FOOT WOUNDS : OUTCOMES SOBERING RESULTS !! NEW SOLUTION = OLD SOLUTION = PREVENTION Education Glycemic control Foot care Early medical tx

28. CREATIVE FOOT AMPUTATIONS FOR HEEL SALVAGE

29. MIDFOOT AMPUTATIONS for failed TMAs, extensive forefoot tissue loss viable, non-infected plantar surface/flap, no Charcot changes Chopart/Lisfranc/variant, no Symes rongeur articular surfaces tarsal bones divide Achilles tendon puncture incision (prevent equinus deformity) no wt bearing 3+ wks

30. ‘CLAM-SHELL’ PROSTHESIS

31. 77 TMAs in 74 patients 32 healed  24/26 functional amb 41 non-healed TMAs  32 midfoot amp + 6 late amps + 9 early amps 23/25 functional amb + 6 early amps

32. MIDFOOT AMPUTATION - PATIENT SELECTION

33. TOP TEN LESSONS / PEARLS / TENETS / PITFALLS 10.Gangrene = severe ischemia, PAD  needs revascularization * * except limited digit gangrene, no infection 9.For patients with PAD, the worse the infection at presentation or the greater the tissue loss, the more normal the arterial supply must be for foot salvage 8. For severe infections with sepsis, the extent of infection/necrosis deep in the foot is always worse than superficial/skin appearance

34. TOP TEN LESSONS / PEARLS / TENETS / PITFALLS 7.Urgent / emergent exploration/debridement for septic foot presentations = priority of controlling local infection 6.For severe infections, use staged debridements/open amps at joints without opening articular surfaces (avoid late osteomyelitis) until final wound closure 5. Prolonged antibiotic therapy is rarely effective for osteomyelitis without resection of bony prominences (neuropathic ulcers) or revascularization for ischemia

35. TOP TEN LESSONS / PEARLS / TENETS / PITFALLS 4.Symes amputation (or any other resecting calcaneus, talus) is not functional 3.Creative/unconventional midfoot amputations are functional & less energy expenditure than proximal amp levels (BKA, AKA) 2. Large heel wounds (involving calcaneus) are most difficult to successfully treat

36. TOP TEN LESSONS / PEARLS / TENETS / PITFALLS 1.The sooner the wound heals / skin closes, the better the outcome … do not pursue prolonged secondary ‘granulation’ healing in large wounds/exposed bone, instead operative debridements and delayed closure !