Current Concepts In Treating Diabetic Foot Wounds

By Richard M. Stillman, MD, FACS Clinical Editor: John Steinberg, DPM

Managing foot wounds in diabetes patients forms much of the core practice of wound care and podiatry. In the United States, the annual cost for the care of diabetic foot wounds exceeds $5 billion.1 It’s been estimated that anywhere from 2.5 to 10.7 percent of patients with diabetes develop a foot wound each year. Even for wounds that heal, the recurrence rate is approximately 55 percent over the next five years. According to one study, the prevalence of neuropathy in the diabetic population is 33.5 percent, the prevalence of vascular disease is 12.7 percent and the prevalence of foot ulcer is 4.75 percent.2 Given these statistics, let’s take a closer look at how the current literature supports (or doesn’t support) our fundamental perceptions about treatment, and examine how the risk of developing foot wounds corrrelates with the patients’ age, height, fasting blood sugar and duration of diabetes. A Few Thoughts About Ulcer Etiology Aside from a previous foot ulcer, the most significant predictor of ulcer occurrence is altered sensation in the foot. Other key etiologic factors include the duration of diabetes, poor control of blood sugars, microvascular problems and structural abnormalities. Microangiopathy tends to occur at a younger age in diabetic patients than in the general population and can lead to neuropathy, nephropathy and retinopathy. Although atherosclerosis is typically diffuse, atherosclerotic disease involving the tibioperoneal vessels (rather than the aortoiliac segment) characterizes the diabetic population. A thickened basement membrane in arterioles and capillaries impairs white cell migration. Microangiopathy leads to neuropathy. Autonomic neuropathy impairs capillary vasodilation in response to injury. Actual occlusion of arterioles is not the problem, a fact attested to by the success of bypass surgery. Neuropathy in the diabetic patient results from abnormalities in the polyol pathway, deficiencies in nerve regeneration and defects of sodium and calcium channels.5 Neuropathy allows repeat episodes of minor trauma to go unnoticed. This results in deformity such as clawing of the toes and collapse of the distal metatarsals and arch, which causes Charcot foot (rocker-bottom deformity). Diabetic patients with a history of foot ulcers have a significantly greater incidence of extension deformity of the first, second and third metatarsophalangeal joints and of arthropathy of the second, third and fourth metatarsophalangeal joints. Interestingly, there is no significant difference in the soft tissue thickness beneath the metatarsal heads or in bone density.6 Many structural abnormalities predispose to diabetic first toe ulcers.7 These include gastrocnemius/soleus equinus, structural hallux limitus, hallux interphalangeal abductus, first ray elevatus or dorsiflexion deformity, functional hallux limitus, interphalangeal joint sesamoid bone, hyperextended interphalangeal joint, prominent plantar-medial condyle of the proximal aspect of the distal phalanx, hallux malleus and metatarsus primus adductus. A Review Of Key Clinical Findings Diabetic ulcers usually occur on the plantar aspect of foot, especially the metatarsal head areas and the tips of the toes. Clinical findings suggesting associated arterial insufficiency include thickened nails, skin atrophy (shiny cool skin), intermittent claudication or pain at rest, pallor on elevation, rubor on dependency, cyanosis, absent pedal pulses and gangrene. Findings characteristic of neuropathy are comprised of abnormalities in response to pinprick, light touch (Semmes-Weinstein monofilaments), vibration, pressure and ankle reflexes. Sensory neuropathy may cause painless ulceration. Motor neuropathy causes muscle atrophy leading to hammertoes, callus formation and ulceration. Autonomic neuropathy, given the absence of sweating, leads to dry skin (xerosis), fissures, bacterial colonization and frank infection. What Is The Current Thinking About Appropriate Workup? Plain X-rays may reveal lytic changes suggestive of osteomyelitis or a necrotizing infection with gas-forming organisms. A three-phase bone scan screens for osteomyelitis, but be aware that current radiopharmaceuticals cannot distinguish accurately between bone infection and soft tissue inflammation.8 Obtaining an MRI may give you useful information about depth of invasion, bone and joint involvement, and associated deformities.9 In one retrospective study, researchers identified abscesses on MRI in 18 percent of patients with osteomyelitis.10 When it comes to assessing the hemodynamic significance of vascular insufficiency, keep in mind that the ankle-brachial pressure index (ABI) is notoriously inaccurate in diabetic patients who have calcification of the arterial media. This calcification prevents compression and causes a falsely elevated index. On the other hand, when you obtain a pulse volume recording (PVR) using a segmental air plethysmograph, it is not affected by calcification and gives a good indication of the hemodynamic significance of arterial disease. Measuring the transcutaneous oxygen tension (TcPO2) can be useful in some cases. A value over 30 mm Hg suggests the wound is likely to heal. When arterial imaging is required for imaging atherosclerotic disease, consider magnetic resonance angiography (MRA) with gadolinium enhancement rather than contrast angiography. After all, radiographic dye is associated with higher risk of renal failure in diabetic patients. However, if contrast angiography is required, remember to institute nephroprotection with hydration and acetylcysteine, and to use a hyposmolar contrast agent. Wound cultures can help you decide about appropriate antibiotic therapy for infected wounds. It has been said that a deep tissue biopsy provides more useful results. However, one study suggests that deep biopsy is no more accurate than superficial swab culture except for wounds that have been infected for over 30 days.11 This study also notes anaerobes are unlikely to grow beyond the first two weeks of antibiotic treatment. After 30 days, gram-positive bacteria predominate. What You Should Know About Treatment Management requires a team approach.12 There are an array of treatments and key considerations in their use. • One key is to treat any infection, which is often polymicrobial. • Remember that offloading is vital and can be accomplished by applying felted foam (for plantar relief reduction) or emphasizing an accomodative dressing, healing shoe, walking splint, crutch-assisted walking or sometimes bed rest. Offloading with total contact casting or non-removable fiberglass proved to be more effective than removable casts or shoes in one study and equally effective in another study.13 • Perform debridement. This may entail abscess drainage, ostectomy, removing callus, exploring undermined areas and removing hidden necrotic tissue. • Use wound dressings that encourage epithelialization such as hydrophilic, alginate and silvadene. Hydrogels seem to be particularly effective.14 • Consider using an FDA-approved topical growth factor. In particular, using a platelet-derived growth factor-BB (PDGF-BB) protein in a cellulose gel (Regranex, becaplermin) achieved a 44 percent healing rate versus 22 percent in the control group in one study.15 However, the cost of this product may be prohibitive for many patients. • Consider performing an excision and random flap closure as a single stage procedure for carefully selected, well-vascularized and very clean ulcers.16 • Consider split thickness skin grafting (STSG) or the use of cultured human dermis (Dermagraft) for intractible but clean wounds. • Don’t forget the importance of glycemic control. Hyperglycemia impairs leokocyte function. When You Should Make A Vascular Referral • In the presence of circulatory impairment, refer the patient for vascular reconstruction. Vascular bypass, especially by the in situ technique for distal occlusions, has been the gold standard. Although graft patency rates are comparable in diabetic and non-diabetic patients, unfortunately the perioperaive mortality rate is significantly higher in the diabetic group.17 Angioplasty, including infrapopliteal angioplasty, turns out to be feasible in many diabetic patients and may indeed be the best primary choice.18 Even angioplasty achieved by subintimal dissection has been effective in certain circumstances.19 Other Options For Difficult Cases In extremely difficult cases, consider less commonly used treatment options. One study advocates surgical decompression of peripheral nerves to restore sensation and relieve pain.20 Athermic laser radiation had a beneficial effect in one study.21 Hyperbaric oxygen therapy (HBO) may be useful for ischemic wounds in which revascularization is not possible or has been unsuccessful. Be aware that the efficacy of HBO correlates best with transcutaneous oxygen tension (TcPO2) measured in the HBO chamber rather than the usual practice of determining eligibility by measuring TcPO2 augmentation outside the chamber.22 Determining The Prognosis Healing time correlates with the size, depth and duration of the initial wound. Wound etiology also provides a valuable predictor of wound healing. Neuropathic ulcers without vascular compromise tend to heal in significantly less time (77 days) than those associated with vascular insufficiency (130 days).23 While infection clearly requires control, in one study at least, the presence of osteomyelitis did not impede wound healing time.24 Patients with impaired renal function are particularly prone to nonhealing and limb loss.25 Amputation is most likely to be required in patients who have other remote diabetic complications such as retinopathy and nephropathy, and those with a low ABI. The latter may respond to vascular reconstruction. Unfortunately, limb salvage after vascular bypass does not necessarily translate into improved ambulation and function.26 Final Notes Diabetic screening and protection programs may reduce the risk of amputation. Interestingly, the evidence is conflicting regarding the efficacy of patient education. One study suggests the benefit of patient education is short-lived (six months) while another study suggests that education has no beneficial effect.27 Insurance may cover prophylactic therapeutic footwear such as extra width and extra length therapeutic shoes with cork, prefabricated inserts or viscoelastic insole. However, there is some question as to the efficacy of widespread dispensing of therapeutic footwear to diabetic patients.28 Active and passive range of motion therapy reduce peak plantar pressures. Therefore, this therapy, theoretically, may help ameliorate the occurrence of foot ulceration.29 Researchers have found that noninvasive surveillance of autologous vascular bypass grafts improves long-term patency rates by identifying potentially failing grafts to allow early repair.30 In summary, diabetic foot ulcers confer a high cost upon society and onerous morbidity upon patients. Focusing on comprehensive multidisciplinary management and prevention is essential in order to help reduce risks and ensure better outcomes. Dr. Stillman (top right) is the Medical Director of the Wound Healing Center and a member of the Board of Trustees of Northwest Medical Center in Margate, Florida. He has published over 100 research papers and textbook chapters, and has authored or edited a half-dozen surgical textbooks. Dr. Steinberg (bottom right) is an Assistant Professor in the Department of Orthopaedics/Podiatry Service at the University of Texas Health Science Center.



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Assessment and management of foot disease in patients with diabetes. N Engl J Med 1994 Sep 29;331(13):854-60 13. Birke JA, Pavich MA, Patout Jr CA, Horswell R. Comparison of forefoot ulcer healing using alternative off-loading methods in patients with diabetes mellitus. Adv Skin Wound Care 2002 Sep-Oct;15(5):210-5 14. Smith J. Debridement of diabetic foot ulcers (Cochrane Review). Cochrane Database Syst Rev 2002;(4):CD003556 15. Pierre A. d’Hemecourt, MD, Chesapeake Research Consultants, Rockville, MD; Janice M. Smiell, MD, M. Reazaul Karim, R.W. Johnson Sodium Carboxymethylcellulose Aqueous-Based Gel vs. Becaplermin Gel in Patients With Nonhealing Lower Extremity Diabetic Ulcers. Wounds 10(3):69-75, 1998 16. Blume PA, Paragas LK, Sumpio BE, Attinger CE. Single-stage surgical treatment of noninfected diabetic foot ulcers. Plast Reconstr Surg 2002 Feb;109(2):601-9 17. Karacagil S, Almgren B, Bowald S, Bergqvist D. Comparative analysis of patency, limb salvage and survival in diabetic and non-diabetic patients undergoing infrainguinal bypass surgery. Diabet Med 1995 Jun;12(6):537-41 18. Faglia E, Mantero M, Caminiti M, CaravaggI C, De Giglio R, Pritelli C, Clerici G, Fratino P, De Cata P, Paola LD, Mariani G, Poli M, Settembrini PG, Sciangula L, Morabito A, Graziani L. Extensive use of peripheral angioplasty, particularly infrapopliteal, in the treatment of ischaemic diabetic foot ulcers: clinical results of a multicentric study of 221 consecutive diabetic subjects. J Intern Med 2002 Sep;252(3):225-32 19. Ingle H, Nasim A, Bolia A, Fishwick G, Naylor R, Bell PR, Thompson MM. Subintimal angioplasty of isolated infragenicular vessels in lower limb ischemia: long-term results. J Endovasc Ther 2002 Aug;9(4):411-6 20. Dellon AL. Preventing foot ulceration and amputation by decompressing peripheral nerves in patients with diabetic neuropathy. Ostomy Wound Manage 2002 Sep;48(9):36-45 21. Schindl A, Schindl M, Schon H, Knobler R, Havelec L, Schindl L. Low-intensity laser irradiation improves skin circulation in patients with diabetic microangiopathy. Diabetes Care 1998 Apr;21(4):580-4 22. Fife CE, Buyukcakir C, Otto GH, Sheffield PJ, Warriner RA, Love TL, Mader J. The predictive value of transcutaneous oxygen tension measurement in diabetic lower extremity ulcers treated with hyperbaric oxygen therapy: a retrospective analysis of 1,144 patients. Wound Repair Regen 2002 Jul-Aug;10(4):198-207 23. Zimny S, Schatz H, Pfohl M. Determinants and estimation of healing times in diabetic foot ulcers. J Diabetes Complications 2002 Sep-Oct;16(5):327-32 24. Hartemann-Heurtier A, Ha Van G, Danan JP, Koskas F, Jacqueminet S, Golmard JL, Grimaldi A. Outcome of severe diabetic foot ulcers after standardised management in a specialised unit. Diabetes Metab 2002 Dec;28(6):477-84 25. Treiman GS, Oderich GS, Ashrafi A, Schneider PA. Management of ischemic heel ulceration and gangrene: An evaluation of factors associated with successful healing. J Vasc Surg 2000 Jun;31(6):1110-8 26. Gardner AW, Killewich LA. Lack of functional benefits following infrainguinal bypass in peripheral arterial occlusive disease patients. Vasc Med 2001;6(1):9-14 27. Valk GD, Kriegsman DM, Assendelft WJ. Patient education for preventing diabetic foot ulceration. A systematic review. Endocrinol Metab Clin North Am 2002 Sep;31(3):633-58 28. Reiber GE, Smith DG, Wallace C, Sullivan K, Hayes S, Vath C, Maciejewski ML, Yu O, Heagerty PJ, LeMaster J. Effect of therapeutic footwear on foot reulceration in patients with diabetes: a randomized controlled trial. JAMA 2002 May 15;287(19):2552-8 29. Goldsmith JR, Lidtke RH, Shott S. The effects of range-of-motion therapy on the plantar pressures of patients with diabetes mellitus. J Am Podiatr Med Assoc 2002 Oct;92(9):483-90 30. 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