The Diabetic Foot
Bonnie Y. Chien, MD
Lew C. Schon, MD, FAAOS
Eric W. Tan, MD, FAAOS
Dr. Schon or an immediate family member has received royalties from Arthrex, Inc., Darco, DJ Orthopaedics, Stryker, and Zimmer; is a member of a speakers’ bureau or has made paid presentations on behalf of Avitus, Paragon 28, and Zimmer; serves as a paid consultant to or is an employee of CurveBeam, Gerson Lehrman Group, Guidepoint Global, MiRus, Paragon 28, and Zimmer; has stock or stock options held in CurveBeam and Parvizi Surgical Innovation; has received research or institutional support from Bioventus and Zimmer; has received nonincome support (such as equipment or services), commercially derived honoraria, or other non-research-related funding (such as paid travel) from Concepts in Medicine LLC, OMEGA, and Smith & Nephew; and serves as a board member, owner, officer, or committee member of the American Academy of Orthopaedic Surgeons. Dr. Tan or an immediate family member is a member of a speakers’ bureau or has made paid presentations on behalf of Arthrex, Inc.; serves as a paid consultant to or is an employee of Arthrex, Inc. and Orbis Medical Devices, Inc.; and serves as a board member, owner, officer, or committee member of the American Academy of Orthopaedic Surgeons and the American Orthopaedic Foot and Ankle Society. Neither Dr. Chien nor any immediate family member has received anything of value from or has stock or stock options held in a commercial company or institution related directly or indirectly to the subject of this chapter.
ABSTRACT
As the incidence and prevalence of diabetes continues to rise, the burden of orthopaedic issues, particularly of the foot, remains a major cause of hospitalizations and morbidity. To effectively manage these issues, a thorough understanding of the systemic effects and consequences of diabetes is imperative. It is important to review the pathophysiology and diagnosis of diabetic foot issues, as well as nonsurgical and surgical treatment options and considerations for this challenging patient population.
Keywords: Charcot arthropathy; diabetic foot; peripheral neuropathy
Introduction
There are an estimated 34.2 million people, or 10.5% of the population in the United States, with diabetes,1 whereas the worldwide burden reaches 463 million adults.2 Direct costs for diabetes care amounted to approximately $237 billion in 2017.3,4 Approximately one-third of individuals with diabetes will experience a foot ulcer at some point in their lives, with nearly 20% requiring an amputation.5 Diabetic foot ulcers precede more than 80% of all nontraumatic amputations. In the United States, there are 108,000 lower extremity amputations performed per year in patients with diabetes.3 The 5-year mortality for Charcot arthropathy and diabetic foot ulcers is estimated to approach approximately 30%, whereas that for minor and major amputations reaches 46.2% and 56.6%, respectively. The diabetic foot is the result of multiple diabetes-related systemic diseases including peripheral sensory neuropathy, peripheral arterial disease (PAD), skin disorders, renal disease, and osteopenia/osteoporosis. Given the scope of the diabetes epidemic, orthopaedic surgeons must not only be able to readily diagnose diabetic foot issues, but perhaps more importantly, to manage the associated complications, ranging from ulceration to infection to Charcot arthropathy.
Peripheral Neuropathy and Vasculopathy
Diabetes is a systemic disease stemming from accumulation of and damage to vasculature by advanced glycation end products, which instigate an inflammatory cascade leading to impaired perfusion and global organ dysfunction.6 Hyperglycemia, insulin resistance, and dysregulation of lipid metabolism induce multiple downstream inflammatory kinases and transcription factors such as nuclear factor kappa B, resulting in proinflammatory cytokine production, including interleukin (IL)-1 B, IL-2, IL-6, and tumor necrosis factor alpha. These cytokines activate cellular oxidative stress that leads to neuronal damage.7 In addition, excess glucose and fatty acids overload energy metabolism
processes in peripheral nerve cells, and toxic substrates accumulate in Schwann cells and dorsal root ganglion neurons, inducing axonal degeneration. It is this peripheral neuropathy that results in the loss of protective sensation; its severity is directly correlated with increased risk of ulceration, amputation, and death. The occurrence rate of distal to proximal, symmetric polyneuropathy in individuals with diabetes is approaching 75%.8 Clinically, the most obvious sign is loss of sensitivity to the Semmes-Weinstein 5.07/10 g monofilament test. Multiple points in the foot can be tested and a global extent of neuropathy can be determined (Figure 1). It is important to note that motor and autonomic nerves can be affected as well. This can cause progressive deformity because of muscle imbalance, altered loading, and trophic and apocrine changes in the skin. Each of these plays an important role in diabetic foot complications.
processes in peripheral nerve cells, and toxic substrates accumulate in Schwann cells and dorsal root ganglion neurons, inducing axonal degeneration. It is this peripheral neuropathy that results in the loss of protective sensation; its severity is directly correlated with increased risk of ulceration, amputation, and death. The occurrence rate of distal to proximal, symmetric polyneuropathy in individuals with diabetes is approaching 75%.8 Clinically, the most obvious sign is loss of sensitivity to the Semmes-Weinstein 5.07/10 g monofilament test. Multiple points in the foot can be tested and a global extent of neuropathy can be determined (Figure 1). It is important to note that motor and autonomic nerves can be affected as well. This can cause progressive deformity because of muscle imbalance, altered loading, and trophic and apocrine changes in the skin. Each of these plays an important role in diabetic foot complications.
 Figure 1 Photograph shows the Semmes-Weinstein monofilament test. The 5.07 value indicates the stiffness of the single-fiber nylon threads that make up the monofilament while 10 g is the force needed to bend it. The 5.07/10 g combination is thought to be the best indicator to determine loss of protective sensation. |
In addition, a common misconception is that patients with neuropathy do not experience pain. The pathogenesis of neuropathic pain is not fully understood. It likely is related to chronic hyperglycemic damage to nerves that can cause an increase in voltage-gated channels that activate nerve potentials and regeneration of nerve sprouts creating neuromas. The expansion of new nerves can damage surrounding nerves and expand the sensitized area via ectopic impulses, leading to a hyperexcited response, both on a peripheral and central nervous system level.9 Neuropathic pain is often bilateral and symmetric, characterized as electric shock-like, burning, and radiating, without necessarily having a trigger. The typical treatment for neuropathic pain is pharmacologic, including selective serotonin reuptake inhibitors and gabapentin or pregabalin.
Furthermore, according to a 2021 study, diabetes is associated with a twofold to sevenfold increase in PAD.10 It can increase the incidence, accelerate the progression, and worsen the severity of PAD. The amputation rate is four times higher than the national average in patients with concomitant diabetes mellitus and PAD.11 With the loss of normal sensory input, motor feedback, vascularity, and autonomic function, the skin can become dry, easily crack, ulcerate, and become infected. Therefore, glycemic level checks establishing proper control of diabetes, foot care, and vascular assessment should be routinely performed.
Diabetic Foot Ulcers and Infection
Risk Factors and Clinical Evaluation
Neuropathy, vasculopathy, and repetitive trauma create a vicious cycle for initial and recurrent ulceration. The highest risk factor for ulceration and infection is history of a previous ulcer.12 Physical examination should include assessment of foot deformity and alignment, areas of contracture or bony prominence that increase plantar pressure, callus or ulceration presence and depth, and the Semmes-Weinstein 5.07 (10 g) monofilament test. Poorly fitting shoes exerting excessive pressure should be noted. An ulcer that can be probed to bone has high sensitivity, specificity, and negative predictive value for osteomyelitis.13
The presence of the dorsalis pedis and posterior tibialis pulses should be clearly documented. If absent, arterial Doppler ultrasonography should be pursued, particularly in the setting of a nonhealing ulcer or if surgical intervention is contemplated. An absolute toe pressure greater than 30 mm Hg has been shown to
be more predictive of healing than the ankle-brachial index, which can be falsely increased by vessel calcification.14,15 In addition, transcutaneous oxygen pressure measurements greater than 40 mm Hg indicate acceptable wound-healing potential.16 If severe vascular compromise is present, a vascular surgeon should be consulted for potential revascularization procedures.
be more predictive of healing than the ankle-brachial index, which can be falsely increased by vessel calcification.14,15 In addition, transcutaneous oxygen pressure measurements greater than 40 mm Hg indicate acceptable wound-healing potential.16 If severe vascular compromise is present, a vascular surgeon should be consulted for potential revascularization procedures.
Grading
The Meggitt-Wagner classification is commonly used for grading ulcers. Stages 0 through 2 are based on increasing ulcer depth without abscess or osteomyelitis, stage 3 represents deep ulcer with abscess or osteomyelitis, whereas stages 4 and 5 denote localized and extensive foot gangrene, respectively. This system is simple to use, has high interrater agreement, and has been validated for healing and need for lower extremity amputation; however, it does not account for PAD or infection, nor provide sufficient prognostic information.17
More recently, the International Working Group on the Diabetic Foot has strongly recommended the SINBAD system for communication about ulcer characteristics. SINBAD is an acronym for site, ischemia, neuropathy, bacterial infection, and depth, and is a reproducible, easy scoring system that is not reliant on any special tests (Table 1). Furthermore, the classification has been validated for ulcer healing and amputation prediction.18
Table 1 SINBAD Classification Creates an Easy Acronym and Scoring System With a Maximum of Six Points for Communication About Diabetic Ulcers | ||||||||||||||||||||||||
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Multidisciplinary Care
Given the systemic effects of diabetes, successful ulcer prevention and treatment involves a multidisciplinary team, including the orthopaedic surgeon, vascular surgeon, plastic surgeon, endocrinologist, infectious disease specialist, nutritionist, as well as the orthotist. Other comorbidities such as hypertension, hyperlipidemia, renal failure, smoking, nutritional status, and glucose control based on hemoglobin A1c should be optimized and rectified to reduce the risks of diabetes-related complications. Hemoglobin A1c reflects glycemic levels over 2 to 3 months and is the standard measure to monitor glycemia, with values ≥6.5% defining diabetes. According to a 2020 systematic review, hemoglobin A1c greater than or equal to 8% and fasting glucose levels greater than or equal to 126 mg/dL have been associated with increased probability of lower extremity amputation in patients with diabetic foot ulcers.19
Nonsurgical Management
Treatment of diabetic ulcers must address abnormal mechanical pressure over the affected area, vascular status, and eradicate infection. The goal is to achieve an ulcer-free and infection-free state as well as enable a shoeable foot in therapeutic footwear with custom inserts and orthotics, as needed.
Wound Care
Without frank abscess or osteomyelitis, most superficial ulcers with necrotic tissue and callus should be sharply débrided to remove any potential nidus for infection and to stimulate the healing response with new granulation tissue. This can be done in the office or clinic setting. This is generally well tolerated because of the patient’s neuropathy. Wet to dry dressings can débride and absorb exudate from draining wounds, whereas moisturizing agents can be added to dried lesions. In addition, a negative-pressure dressing may be needed for persistent ulcers to facilitate healing. Multiple adjuvant treatments are available, including alginates, colloids, and silver-impregnated or iodine-impregnated dressings. Additionally, hyperbaric oxygen therapy is an FDA-approved treatment for nonhealing ulcers.
After débridement, the vulnerable ulcer or callus area should then be appropriately offloaded. Regular evaluation with education on daily skin checks, appropriate shoe wear, and warning signs indicative of local or systemic deterioration should be emphasized.
Orthoses/Shoe Wear
Offloading distributes the mechanical stress across a larger surface area over the foot and prevents shear stresses across vulnerable areas. Total contact casting has been the gold standard with improved healing rates and faster healing time compared with removable walking devices.20 Once the ulcer has reepithelialized using wound care treatments as described previously, long-term appropriate shoe wear is necessary to prevent reulceration and infection. Systematic reviews of footwear and insole designs have demonstrated stronger evidence for rocker soles and moderate evidence for custom insoles to reduce peak plantar pressure.21 Medicare-eligible patients can receive one pair of extra-depth, extra-wide custom shoes and three pairs of custom insoles per year.22 Figure 2 shows different orthoses and supportive shoe wear to protect the diabetic foot in both situations of ulceration as well as deformity.
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