1 UPDATES ON THE MANAGEMENT OF THE DIABETIC FOOT ULCER- WHAT EVERY ENDOCRINOLOGIST SHOULD KNOW Ann M. Zmuda, DPM Associate Professor, Sections of Endocrinology, Vascular Surgery & Orthopedic Surgery
2 Objectives Discuss the prevalence and scope of diabetic foot ulcerations and when to refer Understand the risk factors and physiologic processes leading to ulcerations in the diabetic foot Understand the mechanisms causing ulcer healing impairment in the diabetic foot and how to evaluate these wounds Understand the latest technologies in wound healing for limb salvage
3 Alarming Stats.. There are 25.8 million people in the US with Diabetes (8.3% of the US population and that is estimated to grow to 44 million by 2034) Diabetes is the 7 th leading cause of death in the US with the risk of death among people with diabetes approximately twice that of people without diabetes. Diabetics are 4 times more likely to develop peripheral vascular disease and 5 times more likely to develop critical limb ischemia (CLI) than the general population Up to 25% of patients with a history of DM will develop a foot ulceration 85% of diabetic foot ulcers are preceded by a callus!
4 More stats >60% of non-traumatic lower limb amps occur in people with diabetes 5-15% of diabetics undergo major leg amputations and ~50% of these will either die or lose the contra-lateral limb within 5 years comprehensive foot care/limb salvage programs can reduce amputation rates by 45-85% There has been a shift in amputation levels...
5 University of Iowa Foot and Ankle International Journal dramatic decreases in the number and severity of lower-limb amputations over the past decade Between amputations decreased by 28.8% while surgical orthopedic treatments for ulcers rose by 143% Shift in amputation level: upper and lower leg amputations were down 47% while amputations at the partial-toe level increased by 24% INCREASED MOBILITY, INDEPENDENCE & SURVIVAL RATES!!!!!!!
6 Foot Screening An annual foot screen by a podiatrist is recommended for all low risk diabetic patients. Foot care should be provided by a DPM periodically for those diabetic patients at high risk.
7 Foot Examination Vascular Dorsalis pedis and posterior tibial pulses Neurological 10-gram (5.07 Semmes Weinstein) nylon filament Vibratory sensation Integument/Toe Nails Color, texture, & temperature of skin Hyperkeratotic lesions, helomas, pre-ulcerative lesions, ulcerations Thick toenails which may indicate vascular and/or fungal disease Musculoskeletal Hammer/claw toes, Hallux Valgus, Charcot foot, amputation Biomechanical Foot drop, apropulsive gait,
8 FOOT DEFORMITIES
9 Corns, Calluses, and Preulcerative Lesions
10 So why do our diabetics fail??? long diabetes duration, multiple comorbidities, peripheral neuropathy, peripheral vascular disease, prior foot ulcer, prior foot amputation
11 Wound Healing and Diabetes Three Phases of Wound Healing: 1. Inflammatory 2. Proliferative 3. Remodeling
12 I. INFLAMMATORY PHASE Lasts about 3-4 days from onset of injury. Platelets begin to form clot and produce thrombin which in turn initiates formation of fibrin. Platelets also release growth factors (essential for wound healing). WBC s (neutrophils & macrophages) enter the wound to eliminate bacteria & necrotic tissue and provide defense against infection.
13 II. PROLIFERATIVE PHASE Begins approx. 4 days post injury and usually lasts 3 weeks. Growth factors stimulate mitosis of fibroblasts & other cells (i.e. epithelial). Wound contraction and building of collagen framework takes place. Neovascularization & epithelialization occur.
14 III. REMODELING PHASE Can take up to 2 years to complete! Involves collagen synthesis and breakdown. Goal is to restore functional barrior of skin and increase the tensile strength of the scar.
15 The chronic diabetic foot ulcer is stalled in stage 1: Cessation of epidermal growth & migration over the wound surface. Elevated level of matrix metalloproteinases resulting in increased proteolytic activity and inactivation of growth factors necessary for proper wound healing.
16 Poor response to growth factors Decreased angiogenesis Decreased fibroblast proliferation Altered inflammatory response Decreased energy to cells available for regeneration & activity Decreased collagen production and tensile strength
17 Vascular Disease, Neuropathy,.
18 Anatomic Predisposing Factors of the DF Ulcer The foot only occupies ~2% of the total body surface area, however Most centrifugal portion of the body with dependency Weight bearing; easily traumatized Numerous joints (33), bones (26 total which is ¼ of the bones in the body), & muscles/tendons/ligaments (>100) but less total muscular volume Numerous fibrous septa in the plantar skin Scanty subcutaneous fat in the dorsal skin
19 PHYSICAL EXAMINATION OF THE WOUND Characteristics of the wound: size, shape, color, depth Location Drainage: amount, consistency, quality Odor Associated physical findings
20 Ulcer Treatment There are four basic necessities to obtain healing of these wounds: Vascular Supply: ABI s >.45 diabetic; >.35 nondiabetic Infection Control: I&D, antibiotics Nutrition: Albumin levels >3.5 gm/dl & TLC >1500 cells/cu mm Wound Care: dressings, eliminate pressure
24 Wound Care Technology 1)
25 Cadexomer Iodine Gel is a sterile formulation of Cadexomer Iodine When applied to the wound, Iodosorb cleans it by absorbing fluids, removing exudate, slough and debris and forming a gel over the wound surface. As the gel absorbs exudate, iodine is released, killing bacteria and changing color as the iodine is used up. A 3-in-1 mode of action kills bacteria, manages exudate and debrides the wound bed. IODOSORB
27 SANTYL Collagenase Santyl (collagenase) Ointment is a sterile enzymatic debriding ointment contains 250 collagenase units per gram of white petrolatum USP. The enzyme collagenase is derived from the fermentation by Clostridium histolyticum. It possesses the unique ability to digest collagen in necrotic tissue
28 Fibrotic Base Apply to nickel thickness
33 SNAP Wound VAC System Negative pressure wound therapy
35 KCI WOUND VAC SYSTEM V.A.C. Therapy promotes wound healing through Negative Pressure Wound Therapy (NPWT). By delivering negative pressure (a vacuum) at the wound site through a patented dressing, this helps draw wound edges together, remove infectious materials and actively promote granulation.
36 ALGINATE DRESSINGS Highly absorbent, biodegradable Derived from seaweed The high absorption is achieved via strong hydrophilic gel formation which limits wound secretions and minimizes bacterial contamination Alginate dressings maintain a physiologically moist microenvironment that promotes healing and the formation of granulation tissue. Alginates can be rinsed away with saline irrigation, so removal of the dressing does not interfere with healing granulation tissue. Alginate dressings are very useful for moderate to heavily exudating wounds
37 Venous Stasis Wounds
38 VERSAJET SYSTEM Reduced bacterial burden Preserves viable tissue Removes unwanted necrosis and debris Improved graft and synthetic dressing results
39 APLIGRAF Living, bi-layered skin substitute Lower dermal layer combines bovine type 1 collagen and human fibroblasts Upper epidermal layer is formed by promoting human keratinocytes to multiply and differentiate No hair follicles, sweat glands, melanocytes, macrophages, or lymphocytes Developed by Organogenesis
40 Porcine small intestine sub-mucosa A 3-dimensional, bioresorbable extracellular matrix (ECM), that is incorporated and absorbed into the wound Can graft over exposed tendon and bone 3 year shelf life OASIS
42 REGRANEX Platelet derived growth factor For use in granular wounds to decrease time to closure Active in all phases of wound healing: Initiates macrophage activity Chemotactic for fibroblasts Promotes angiogenesis Wound contracture Re-epithelialization New collagen formationn Must be refrigerated!!!
43 Application of Regranex July 26-September 20
44 EPIFIX Biologic Human Amniotic Membrane allograft Comprises the innermost layer of the placenta and lines the amniotic cavity Histologically, the amniotic membrane is non-vascular & consists of epithelium cells, basement membrane, and a fibrous layer containing cell anchoring collagen types Serves as a biologically active implant or graft for tissue regeneration application Developed by MiMedx Group
48 HEEL ULCERATIONS
49 INFECTIONS The microbiology of diabetic foot wounds is variable depending on the extent of involvement Superficial diabetic foot infections are likely to be aerobic gram-positive cocci (S. aureus, S. pyogenes, S. agalactiae, coagulase-negative staphylococci) Deep ulcers, chronically infected &/or previously treated with antibiotics are usually polymicrobial (in addition to Staph - Enterococci, Pseudomonas, Enterobacteriaceae, & anaerobes) Wounds with necrosis/gangrene, & extensive local inflammation should be presumed anaerobic as well as the above
51 Soft Orthotics - Thermoplastic Orthotics
52 SHOES, SHOES, SHOES, SHOES...
53 FREE SHOES!!! Diabetic patients on Medicare are entitled to receive one free pair of shoes and 2 free pairs of insoles every year. Write the prescription, the patient goes to the lab, and they make the shoes as well as bill the insurance. Certificate of medical necessity.
55 If you are going through hell, keep going! Winston Churchill
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