Introduction
Diabetic foot ulcers (DFUs) precede 85% of nontraumatic lower extremity amputations (LEAs). Approximately 3-4% of individuals with diabetes currently have foot ulcers or deep infections.
Semmes-Weinstein 5.07 (10 g) monofilament; the monofilament is applied to the high-risk areas on the plantar surface of the foot (ie, toe pulps, metatarsal heads, heel). Patients who cannot feel pressure from the monofilament have lost protective sensation and are at risk of developing a diabetic foot ulcer.
Among persons with diabetes, 15% develop foot ulcers during their lifetime. Their risk of LEA increases by a factor of 8 once an ulcer develops. At 2 years following transtibial amputation, 36% of these patients are known to have died.
Problem
Individuals who develop foot ulcers have a decided health-related decrease in their quality of life and consume a great deal of health care resources.
Frequency
Among persons with diabetes, 15% develop diabetic foot ulcers (DFUs) during their lifetimes. Currently, 3-4% of individuals with diabetes have deep infections or DFUs.
Etiology
Peripheral neuropathy
Peripheral neuropathy affects sensory, motor, and autonomic pathways. Sensory neuropathy deprives the patient of early warning signs of pain or pressure from footwear, from inadequate soft-tissue padding, or from infection. This neuropathy appears in a stocking-glove distribution, with many patients complaining of burning or searing pain.1
Optimal control of blood glucose levels decreases the incidence of most diabetes-associated organ system morbidity. The primary risk factor for the development of diabetic foot ulcers (DFUs) is loss of protective sensation, best measured by insensitivity to the Semmes-Weinstein 5.07 (10 g) monofilament (see Image 1). Abnormal white blood cell (WBC) function and the presence of peripheral vascular disease allow wounds to become contaminated and infected by organisms that normally are nonpathogenic. This explains the identification of unusual bacteria from the wounds of patients with diabetes.
Semmes-Weinstein 5.07 (10 g) monofilament; the monofilament is applied to the high-risk areas on the plantar surface of the foot (ie, toe pulps, metatarsal heads, heel). Patients who cannot feel pressure from the monofilament have lost protective sensation and are at risk of developing a diabetic foot ulcer.
Autonomic neuropathy produces chronic venous swelling. Motor peripheral neuropathy or Charcot arthropathy can produce bony deformity, which, combined with the loss of protective sensation, can result in skin ulceration from pressure or from shear forces. Associated factors are a history of foot infection or ulceration and previous partial or whole-foot amputation.
Motor neuropathy leads to muscle weakness and intrinsic muscle atrophy in the hands and feet. Patients with motor neuropathy can develop bunion, claw toe, and hammertoe deformities as a result of muscle imbalance. They lose normal vascular tone and thermal regulation, often developing severe venous swelling that can be managed only with compression hose. Severe tissue swelling can lead to ulceration and infection. The patients develop dry, cracked skin as a result of autonomic dysfunction, with the cracks allowing the entry of bacteria. Nail deformity or pathologic proliferation may make the areas adjacent to the nails foci for skin breaks or for infection.
Vascular disease
Ischemic peripheral vascular disease is the second risk factor for developing diabetic foot ulcer and infection. This disorder used to be considered a small vessel disease, but current research links the vascular pathology to the basement membrane of the arterial wall. The characteristics of the disease are similar in persons who are diabetic and those who are not, except that its distribution is somewhat more scattered and geographic in persons who are not diabetic, as opposed to being progressive in a distal direction in persons who are diabetic.
Immune deficiency
The third major risk factor is related to the immune deficiency seen in persons with diabetes. Glycosylated immune proteins lose efficiency, and granulocytes do not perform adequately, leaving these patients prone to infection with organisms that would not affect a healthy host.
Each of these potential abnormalities make the diabetic foot susceptible to abnormal mechanical stresses that can lead to a break in the normal soft-tissue envelope. This can initiate a foot infection that cannot be resolved easily.
Pathophysiology
Pressure over a bony prominence has often been cited as the cause for skin breakdown in patients with diabetes. Skin breakdown occurs at far lesser loads when the pressure is applied by shear forces. The accompanying loss of protective sensation prevents the patient from being warned that intolerable loads have been applied. This leads to blister formation and full-thickness skin loss. The process is heightened in the presence of severe venous swelling, which further lowers the injury threshold. Shoes become tight due to swelling, thus increasing the direct pressure and shear forces applied to skin overlying the bony prominence. Thickened, hypertrophic nails increase pressure on the soft tissues surrounding the nails. The common result is tissue failure and ulcer formation.
Once the skin barrier is broken, wound healing can be impaired by abnormally functioning WBCs. Moreover, patients often are malnourished. Many have a marginal vascular supply, with less ability to achieve resolution of infection and wound healing.
Presentation
Classification of diabetic foot ulcers
Most experts use some variant of the classification system developed by Wagner and most currently modified by Brodsky.2,3
Table 1. Depth-Ischemia Classification of Diabetic Foot Lesions*2
Open table in new window
Table
| Depth Classification | Definition | Treatment |
|---|---|---|
| 0 | At-risk foot, no ulceration | Patient education, accommodative footwear, regular clinical examination |
| 1 | Superficial ulceration, not infected | Offloading with total contact cast (TCC), walking brace, or special footwear |
| 2 | Deep ulceration exposing tendons or joints | Surgical debridement, wound care, offloading, culture-specific antibiotics |
| 3 | Extensive ulceration or abscess | Debridement or partial amputation, offloading, culture-specific antibiotics |
| Ischemia Classification | ||
| A | Not ischemic | |
| B | Ischemia without gangrene | Noninvasive vascular testing, vascular consultation if symptomatic |
| C | Partial (forefoot) gangrene | Vascular consultation |
| D | Complete foot gangrene | Major extremity amputation, vascular consultation |
| Depth Classification | Definition | Treatment |
|---|---|---|
| 0 | At-risk foot, no ulceration | Patient education, accommodative footwear, regular clinical examination |
| 1 | Superficial ulceration, not infected | Offloading with total contact cast (TCC), walking brace, or special footwear |
| 2 | Deep ulceration exposing tendons or joints | Surgical debridement, wound care, offloading, culture-specific antibiotics |
| 3 | Extensive ulceration or abscess | Debridement or partial amputation, offloading, culture-specific antibiotics |
| Ischemia Classification | ||
| A | Not ischemic | |
| B | Ischemia without gangrene | Noninvasive vascular testing, vascular consultation if symptomatic |
| C | Partial (forefoot) gangrene | Vascular consultation |
| D | Complete foot gangrene | Major extremity amputation, vascular consultation |
*Adapted from Brodsky JW: The diabetic foot. In: Coughlin MJ, Mann RA, eds. Surgery of the Foot and Ankle. St Louis, Mo: Mosby; 1999: 911.
Indications
From a practical standpoint, vascular surgery consultation is warranted only when the patient is symptomatic with ischemic pain or a nonhealing ulcer. Ischemic ulcers generally require angioplasty or vascular bypass surgery to achieve wound healing. Neuropathic ulcers require debridement of nonviable or infected tissue, combined with local wound care and offloading.
Grade 3 ulcers require debridement of infected or gangrenous tissue. Partial foot amputation, more complex offloading or non — weight bearing, and culture-specific parenteral antibiotic therapy are necessary. Grade 4 ulcers require partial or whole foot amputation.
Relevant Anatomy
See Medical Therapy.
Contraindications
The 1 or 2 elective issues in this topic are clearly indicated within the text. Most of the substance of this chapter is nonsurgical. Failure to follow the guidelines discussed here leads to deep infection and amputation.
More on Diabetic Foot |
 Overview: Diabetic Foot |
| Workup: Diabetic Foot |
| Treatment: Diabetic Foot |
| Follow-up: Diabetic Foot |
| Multimedia: Diabetic Foot |
| References |
| Further Reading |
| Next Page » |
References
Bengtsson L, Jonsson M, Apelqvist J. Wound-related pain is underestimated in patients with diabetic foot ulcers. J Wound Care. Oct 2008;17(10):433-5. [Medline].
Brodsky JW. The diabetic foot. In: Coughlin MJ, Mann RA, eds. Surgery of the Foot and Ankle. St Louis, Mo: Mosby; 1999:895-969.
Wagner FW Jr. Management of the diabetic neurotrophic foot part II. A classification and treatment program for diabetic, neuropathic, and dysvascular foot problems. In: Instructional Course Lectures: The American Academy of Orthopaedic Surgeons. vol 28. St Louis, Mo: 1979:143-65.
Rozzanigo U, Tagliani A, Vittorini E, Pacchioni R, Brivio LR, Caudana R. Role of magnetic resonance imaging in the evaluation of diabetic foot with suspected osteomyelitis. Radiol Med. Oct 25 2008;[Medline].
Smieja M, Hunt DL, Edelman D, et al. Clinical examination for the detection of protective sensation in the feet of diabetic patients. International Cooperative Group for Clinical Examination Research. J Gen Intern Med. Jul 1999;14(7):418-24. [Medline].
Perkins BA, Olaleye D, Zinman B, et al. Simple screening tests for peripheral neuropathy in the diabetes clinic. Diabetes Care. Feb 2001;24(2):250-6. [Medline]. [Full Text].
Peripheral arterial disease in people with diabetes. Diabetes Care. Dec 2003;26(12):3333-41. [Medline]. [Full Text].
Armstrong DG, Lipsky BA. Diabetic foot infections: stepwise medical and surgical management. Int Wound J. Jun 2004;1(2):123-32. [Medline].
Lipsky BA, Berendt AR, Deery HG, et al. Diagnosis and treatment of diabetic foot infections. Plast Reconstr Surg. Jun 2006;117(7 Suppl):212S-38S. [Medline].
Rao N, Lipsky BA. Optimising antimicrobial therapy in diabetic foot infections. Drugs. 2007;67(2):195-214. [Medline].
Pinzur MS, Slovenkai MP, Trepman E. Guidelines for diabetic foot care. The Diabetes Committee of the American Orthopaedic Foot and Ankle Society. Foot Ankle Int. Nov 1999;20(11):695-702. [Medline].
Singh N, Armstrong DG, Lipsky BA. Preventing foot ulcers in patients with diabetes. JAMA. Jan 12 2005;293(2):217-28. [Medline]. [Full Text].
Cavanagh PR, Lipsky BA, Bradbury AW, et al. Treatment for diabetic foot ulcers. Lancet. Nov 12 2005;366(9498):1725-35. [Medline].
Reiber GE, Lipsky BA, Gibbons GW. The burden of diabetic foot ulcers. Am J Surg. Aug 1998;176(2A Suppl):5S-10S. [Medline].
White R, McIntosh C. Topical therapies for diabetic foot ulcers: standard treatments. J Wound Care. Oct 2008;17(10):426, 428-32. [Medline].
Lipsky BA, Holroyd KJ, Zasloff M. Topical versus Systemic Antimicrobial Therapy for Treating Mildly Infected Diabetic Foot Ulcers: A Randomized, Controlled, Double-Blinded, Multicenter Trial of Pexiganan Cream. Clin Infect Dis. Nov 6 2008;[Medline].
Cabeza de Vaca FG, Macias AE. Wound care for salvaging diabetic foot. J Hosp Infect. Oct 23 2008;[Medline].
Myerson M, Papa J, Eaton K, et al. The total-contact cast for management of neuropathic plantar ulceration of the foot. J Bone Joint Surg Am. Feb 1992;74(2):261-9. [Medline].
Ali R, Qureshi A, Yaqoob MY, Shakil M. Total contact cast for neuropathic diabetic foot ulcers. J Coll Physicians Surg Pak. Nov 2008;18(11):695-8. [Medline].
Ulbrecht JS, Wukich DK. The Charcot foot: medical and surgical therapy. Curr Diab Rep. Dec 2008;8(6):444-51. [Medline].
Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation. Basis for prevention. Diabetes Care. May 1990;13(5):513-21. [Medline].
Pinzur MS, Gottschalk F, Smith D, et al. Functional outcome of below-knee amputation in peripheral vascular insufficiency. A multicenter review. Clin Orthop. Jan 1993;(286):247-9. [Medline].
Further Reading
Clinical trials
Randomized, Controlled Multicenter Trial of Vacuum Assisted Closure Therapy™ in Diabetic Foot Ulcers
FDG-PET Imaging in Complicated Diabetic Foot
Study Evaluating the Safety and Efficacy of a Once-Daily Dose of Tigecycline vs Ertapenem in Diabetic Foot Infections
Clinical Trial for the Treatment of Diabetic Foot Ulcers Using a Nitric Oxide Releasing Patch: PATHON
Evaluation of the Effect of Vivostat Platelet Rich Fibrin(PRF) in the Treatment of Diabetic Foot Ulcers
A Prospective Study of Endothelial Dysfunction and Diabetic Foot Ulcer Risk
Clinical guidelines
Assessment and management of foot ulcers for people with diabetes. Registered Nurses Association of Ontario - Professional Association. 2005 Mar. 112 pages. NGC:004216
Clinical guidelines for type 2 diabetes. Prevention and management of foot problems. National Collaborating Centre for Primary Care - National Government Agency [Non-U.S.]. 2004 Jun 17. 103 pages. NGC:003546
Diagnosis and treatment of diabetic foot infections. Infectious Diseases Society of America - Medical Specialty Society. 2004 Oct 1. 26 pages. NGC:003874
Related eMedicine topics
Diabetes Mellitus, Type 1
Diabetes Mellitus, Type 2
Diabetic Foot Infections
Amputations of the Lower Extremity
Gait Analysis After Amputation
Keywords
diabetic foot, Charcot foot, diabetic foot ulcer, DFU, DFUs, diabetic neuropathy, peripheral neuropathy, ischemic peripheral vascular disease, diabetic foot infection, diabetic heart disease, Charcot osteoarthropathy, Charcot arthropathy, hypertrophic osteoarthropathy, foot amputation, LEA, LEAs, lower extremity amputation, wound infection
