Diabetic Foot

Chapter 85 Diabetic Foot

An estimated 25.8 million children and adults in the United States have diabetes. This makes up 8.3% of the population and includes 18.8 million people with diagnosed diabetes, 7 million who are undiagnosed, and 79 million who are prediabetic. Medical costs for patients with diabetes were estimated to be $174 billion in 2007, with expenses being 2.3 times higher for patients with diabetes than for those without. Diabetic patients are prone to foot and ankle problems for multifactorial reasons.

Risk Factors for Foot Problems in Diabetic Patients

Peripheral Neuropathy

Increased blood glucose levels cause nerve damage by multiple pathways. Different metabolic pathways are activated by the excess glucose, leading to excess reactive oxygen species (ROS), such as nitric oxide and hydrogen peroxide, and advanced glycosylation end products, such as hemoglobin A1c. ROS cause damage by causing nerve ischemia, affecting protein and cell lipids, and injuring nuclear material, leading to increased apoptosis. Advanced glycosylation end products, by binding cellular receptors and causing other metabolic shifts, decrease the cell’s ability to detoxify itself. Nerve myelinization also can be affected, along with injury to nerve ion channels, which can decrease conduction velocity and increase pain impulses. Microvascular disease also can cause damage to nerves.

When large sensory nerve fibers are affected, protective sensation can be lost. Small fiber afferent neuropathy can lead to increased pain generation. Motor neuropathy can cause foot deformities, such as claw toes, which can lead to ulcerations over bony prominences. When the sympathetic nervous system is affected, the skin becomes dry and scaly, eventually causing cracks in the skin through which bacteria can enter to cause infections.

Peripheral neuropathy can be diagnosed by physical examination and can be confirmed with electromyography/nerve conduction studies. Sixty to 70 percent of patients with diabetes have some neural manifestation, and almost 30% of patients with diabetes who are 40 years or older have loss of sensation in the feet. Loss of protective sensation can be determined by use of a 5.07-mm Semmes-Weinstein filament and is thought to be the threshold at which complications such as neuropathic ulcers and Charcot arthropathy occur (Fig. 85-1).

Diabetic Ulcers and Infections

Care of diabetic foot ulcers and their complications has been estimated to cost more than 10 billion dollars a year. Diabetic ulcers can have a significant impact on the patients’ quality of life: patients with unhealed ulcers have lower scores than those with healed ulcer, and both have lower scores than the general population.


Nonoperative Treatment

Total contact casting is the standard of care, because it reduces plantar loads better than a well-molded shoe cast and, by extrapolation, better than shoes with custom insoles (Fig. 85-7). Complications may arise from the use of total contact casts, but most are minor and reversible new areas of ulcerations. The risk for complications of total contact casting is lower after deformity-correcting surgery, as well as when the patient is non–weight bearing. Trepman et al. described a method for total contact casting (Fig. 85-8). In a patient who cannot be kept non–weight bearing, the addition of a metal stirrup that extends beyond the foot-plate of the cast takes pressure off the plantar surface of the foot and transmits it to the shank of the cast (Fig. 85-9). Healing rates after total contact casting can be high; however, the recurrence rate also can be high unless severe deformities are surgically corrected.

Removable diabetic boots (Fig. 85-10) have been shown to be as efficacious as total contact casting in some studies; however, in one study, whereas the boot demonstrated better forefoot unloading than a total contact cast, healing rates were better in the cast, presumably secondary to lack of patient compliance with the boot. Wrapping the diabetic boot to make it less removable does lead to healing rates that are higher than boots that are not wrapped, again suggesting that patient compliance is an issue with the removable boot.

Negative pressure wound treatment with vacuum-assisted closure can improve wound healing. Immediate abscess evacuation with débridement or partial amputation as needed, followed by placement of negative pressure wound therapy, along with vascular intervention as required, can be successful for limb salvage in patients with severe diabetic foot infections. Negative-pressure wound therapy also can be beneficial for diabetic ulcer healing, with higher healing rates and lower amputation rates than advanced moist wound therapy.

Hyperbaric oxygen treatment has been shown in multiple studies to have some efficacy in diabetic wound healing, with an overall healing rate of 76% compared with 48% without the use of hyperbaric oxygen and an amputation rate of 19% compared with 45% without hyperbaric oxygen. It also can be helpful in wound healing when infection is involved. The effect of hyperbaric oxygen is dose dependent: a lower amputation rate is achieved with more than 10 sessions compared with that obtained with fewer than 10 sessions.

Extracorporeal shockwave treatment can be helpful for healing of chronic ulcers and has been shown in one study to be more successful for healing ulcers than hyperbaric oxygen treatment.

If a diabetic foot ulcer becomes infected, antibiotic therapy should be instituted; because no specific regimen has been proven to be effective, consultation with an infectious disease specialist may be helpful. Empirical therapy often is required because superficial swabs often yield contaminants. Deep cultures obtained after débridement can be helpful to direct antibiotic therapy.

Operative Treatment

According to guidelines based on a systematic review by the International Working Group on the Diabetic Foot, the indications for urgent surgical intervention include necrotizing infections and gangrene or deep abscesses (Fig. 85-11). Less urgent surgery may be required if there is a substantially compromised soft tissue envelope, loss of mechanical function of the foot, or bone involvement that is limb threatening or if the patient prefers to avoid prolonged antibiotic therapy. Surgical débridement of osteomyelitis is not always required.

For severe infections with abscess formation, incision and drainage with thorough débridement may be required. In cases of chronic osteomyelitis that has failed to respond to intravenous antibiotics, surgical débridement may be necessary. Infected bone should be completely excised; however, every effort should be made to preserve as much bone as possible. For osteomyelitis in the toes, amputation may be required. Preservation of part of the proximal phalanx may help keep the adjacent toes from drifting (Fig. 85-12).

Osteomyelitis of the metatarsal heads is relatively common (Fig. 85-13) because many ulcers occur in this area.Metatarsal head resection may be indicated. If multiple metatarsal heads are involved, resection of all lesser metatarsal heads or transmetatarsal amputation may be required. Ray resection may be needed if the osteomyelitis involves more than the metatarsal head. Midfoot osteomyelitis can be treated with exostectomy if stability can be preserved. Hindfoot infections occasionally can be treated with amputation at that level, but a below-knee amputation often is more functional. Partial calcanectomy may be attempted if osteomyelitis affects the calcaneus secondary to a heel ulcer and can avoid a below-knee amputation.

Modified resection arthroplasty after débridement of infected tissue can avoid toe amputation in patients with chronically infected ulcers and claw toe deformities (Fig. 85-14), and toe flexor tenotomies can lead to healing of ulcers at the tip of the toe if the claw toe deformity is flexible and wounds are Wagner grade 1, 2, or 3. For chronic infected ulcers under the first metatarsal head, ray resection may be avoided with resection of the first metatarsophalangeal joint and pin stabilization.

Plantar pressures are increased in patients with diabetes. Achilles lengthening can decrease these pressures and can help ulcer healing. Healing of forefoot ulcers can be helped by tendon lengthenings using gastrocsoleus recession for all forefoot ulcers and adding an intramuscular lengthening of the posterior tibial tendon for fifth metatarsal head ulcers and Z-type lengthenings of the peroneus longus tendon for first metatarsal head ulcers.

Charcot Arthropathy


The diagnosis of Charcot arthropathy usually can be made by physical examination and radiographs. The erythema, warmth, and swelling may be mistaken for infection; however, with infection these signs do not decrease with elevation. With infection, glucose control may become difficult, which is not the case in a patient with Charcot arthropathy. With Charcot arthropathy, the patient usually feels well otherwise, which may not be the case with infection.

The diagnostic dilemma occurs when Charcot arthropathy is accompanied by ulceration and possible infection. Imaging studies such as plain radiographs, CT scans, and bone scans can be positive in both Charcot arthropathy and osteomyelitis (Fig. 85-16). White blood cell scans can be helpful, especially when combined with sulfur colloid bone marrow imaging. If infection is present, the tagged white cells will accumulate at the site but the sulfur colloid scan will be negative because bone marrow activity will be depressed by the infection. It does, however, take about 1 week for the sulfur colloid scan to be negative after the onset of infection. Positron emission tomography can be very sensitive and specific, but this test is not widely available. It also can be difficult to differentiate between Charcot arthropathy and infection on MRI; MRI characteristics of sinus tract, replacement of soft tissue fat, fluid collection, and extensive bone marrow abnormality may indicate infection in a patient with Charcot arthropathy. Thin rim enhancement of effusion, subchondral cysts, and intraarticular bodies suggest a lack of infection.

Jun 5, 2016 | Posted by in ORTHOPEDIC | Comments Off on Diabetic Foot
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