Dr. Frykberg is podiatry chief and residency director and Dr. Banks is a research fellow, both at the Phoenix VA Health Care System in Arizona. Dr. Frykberg is a professor of practice at the University of Arizona College of Medicine in Phoenix. Dr. Banks is a professor at Grand Canyon University in Phoenix.
Author disclosures Dr. Frykberg has received research support from Osiris Therapeutics, Advanced BioHealing, AOTI, KCI, Smith & Nephew, Tissue Regenix, and ACell. All other authors report no actual or potential conflicts of interest with regard to this article.
Disclaimer The opinions expressed herein are those of the authors and do not necessarily reflect those of Federal Practitioner, Frontline Medical Communications Inc., the U.S. Government, or any of its agencies. This article may discuss unlabeled or investigational use of certain drugs. Please review the complete prescribing information for specific drugs or drug combinations—including indications, contraindications, warnings, and adverse effects—before administering pharmacologic therapy to patients.
The prevalence of diabetes mellitus (DM) is growing at epidemic proportions in the U.S. and has been reported as the most common reason for hospital admissions in western countries.1 There continues to be an alarmingly steady increase in the incidence of type 2 DM (T2DM), especially among the young and obese. Long-term diabetes-related complications also are likely to rise in prevalence. In particular, the diabetic foot is associated with morbidity and disability, leading to a significant impairment of quality of life.2 People with DM develop foot ulcers because of neuropathy (sensory, motor, and autonomic deficits), ischemia, or both.3 The initiating injury may be from acute mechanical or thermal trauma or from repetitively or continuously applied mechanical stress.4
From foot ulcerations to neuropathy to peripheral vascular disease, the challenges are significant and can result in amputations and even premature death. To address these challenges, early diagnosis and a multidisciplinary team approach should be employed. Managing the numerous comorbidities is essential for treatment.1,2,5
Due to the longevity of patients with DM, diabetes-associated complications are expected to rise in prevalence.6 The American Diabetes Association recently reported that T2DM accounts for about 90% to 95% of all persons with DM.7,8 Today, many hospitalizations for patients with DM are for lower extremity conditions, such as ulceration, infection, or gangrene. Diabetic foot ulcerations (DFUs) are painful and costly for both the patient and the health care system. Every year, more than 1 million people with DM worldwide lose a leg as a consequence of this disease.9 Most DM-related amputations are preceded by a foot ulcer.
Diabetic foot ulcerations are the most common foot condition leading to lower extremity amputation (Figure 1).10 About 14 million individuals in the U.S. with diagnosed and undiagnosed DM will experience pathologic changes of their lower extremities that, when combined with minor trauma and infection, may lead to serious foot problems.11 Although the triad of vasculopathy, neuropathy, and susceptibility to infection are the primary permissive factors in its pathogenesis, DFU can also be attributed to other important risk factors. The presence of peripheral neuropathy and peripheral arterial disease (PAD) are considered to be the most significant risk factors for all types of diabetic foot complications.12
Optimal care of foot ulceration depends on the treating physician’s understanding of the pathophysiology involved, familiarity with accepted principles of treatment, and the knowledge that a coordinated, multidisciplinary team approach will best accomplish the goal of limb salvage. All efforts should be made to prevent foot lesions, and when present, existing ulcers should be treated promptly and aggressively, which can often prevent an exacerbation of the problem and decrease the incidence of amputations. Even when ulcers have healed, patients with DM and a history of a lower extremity ulcer should consider it a lifelong condition that requires monitoring to prevent recurrence.13,14
This review provides a brief overview of DFU, including etiology, evaluation, treatment, and prevention, to provide clinicians with the clinical markers, evidence, and DFU treatment recommendations.
Etiologies
Multiple risk factors contribute to the development and pathogenesis of DFUs.5,6,15,16 Neuropathy and PAD are major factors in the pathogenesis of diabetic foot ulcers.17 However, there are several additional factors leading to the occurrence of foot complications. Reiber and colleagues have determined that 63% of their patients’ ulcers were attributed to the critical triad of peripheral sensory neuropathy, trauma, and deformity.15
Other factors also implicated in the causal pathway to ulceration were ischemia, callus, and edema. Infection was rarely implicated in the etiology of these lesions, although once an ulcer has developed, infection and PAD were found to be the major causes for amputation.10,18,19 Many of the risk factors for foot ulcer are also predisposing factors for amputation, because ulcers are primary antecedent events leading to amputation.20-23
Other contributing causes for ulceration that have been identified are gender (male), duration of DM longer than 10 years, advanced age, high body mass index, prior ulceration, and other comorbidities, such as retinopathy, glycated hemoglobin level, limited joint mobility, foot deformity (Charcot foot, prior partial foot amputation, etc), high plantar pressures, and inappropriate foot self-care habits (Table 1).3-6,22,24,25
Evaluation
The clinical evaluation must include a thorough and systematic lower extremity examination when starting DFU treatment. It is important to have a thorough assessment of the ulcer’s size and depth, and the evaluation should include a description of its appearance and measurement of its diameter at each visit. Evaluation for the presence of local and systemic infection and potential for osteomyelitis, using a small sterile blunt probe, is critical in determining depth of penetration and tracking along tendon sheaths (Figure 2).
Directly probing to bone (positive probe to bone test) has a high predictive value for underlying osteomyelitis even without acute signs of infection.26 In addition, inspecting the wound for gangrene, necrosis, cellulitis, or infection and inspection of shoes for proper fit, foreign objects, and wear patterns can provide insight into other complications and underlying issues.
