Optimal control of blood glucose decreases the incidence of most diabetes-associated organ system morbidity. The primary risk factor for the development of 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 function and the presence of peripheral vascular disease allow wounds to become contaminated and infected by normally nonpathogenic organisms. This explains the identification of unusual bacteria from the wounds of patients with diabetes.

Autonomic neuropathy produces chronic venous swelling. Motor peripheral neuropathy or Charcot osteoarthropathy can produce bony deformity, which, combined with the loss of protective sensation, can produce skin ulceration from pressure or from shear forces. Associated factors are 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. These patients can develop bunion, claw toe, and hammertoe deformities due to 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. They develop dry cracked skin due to autonomic dysfunction. This skin is prone to developing 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.

Ischemic peripheral vascular disease is the second risk factor for developing diabetic foot ulcer and infection. This used to be considered a small vessel disease, but current research links the vascular pathology to the basement membrane of the arterial wall. The disease is similar to that in those with vascular disease who are not diabetic, except that the distribution is somewhat more scattered and geographic in persons who are not diabetic, as opposed to progressive in a distal direction in persons who are diabetic.

The third major risk factor is related to the immune deficiency seen in this patient population. Glycosylated immune proteins lose efficiency, and granulocytes do not perform adequately, leaving these patients prone to infection from 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, which can initiate a foot infection that cannot be resolved easily.

Pathophysiology: Pressure over bony prominence often has 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 bony prominence. Thickened hypertrophic nails increase pressure to 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 white blood cells. These patients often are malnourished. Many have marginal vascular supply, with less ability to achieve resolution of infection and achieve wound healing.

Clinical:
 

Classification of diabetic foot ulcers

Most experts use some variant of the classification system developed by Wagner and most currently modified by Brodsky.

Table 1. Depth-Ischemia Classification of Diabetic Foot Lesions*

*Adapted from Brodsky, J: The Diabetic Foot. In Surgery of the Foot and Ankle, Coughlin, MJ, and Mann, RA, editors. Mosby Inc., St. Louis, 1999. Table 21-2, page 911.

Contraindications: The one or two elective issues in this topic are clearly indicated within the text. Most of the substance of this chapter is nonsurgical. Failure to follow these guidelines leads to deep infection and amputation.

Medical therapy:
Preventive strategies

The major focus of current diabetic foot care is prevention. Preventive strategies combine patient education, prophylactic skin and nail care, and protective footwear. Foot-specific individualized patient education is the most important element of a comprehensive diabetic foot program. Low-risk individuals must wear nonconstrictive shoes. Soft leather or athletic footwear decreases the risk of tissue breakdown from direct pressure. Cushioned stockings are helpful, and white socks make identification of skin breakdown easier, especially in individuals with impaired vision. Nails should be cut transversely to decrease the risk of an ingrown toenail. Once a problem arises, the patient is instructed to seek medical attention immediately. Often, the earliest sign of infection is slowly increasing blood sugars and insulin requirement.

When applied to diabetic populations, these preventive programs have been shown to markedly decrease the rates of DFU and LEA.

When individuals progress to a higher degree of risk, they require accommodative footwear and prophylactic skin and nail care. Depth-inlay soft leather laced oxford shoes with accommodative pressure and shear-dissipating custom foot orthoses (insoles) have been shown to appreciably decrease the development of a DFU. The complexity and individualized nature of the shoes and custom foot orthoses vary with the magnitude of deformity and loss of protective sensation. Calluses should be pared to decrease the incidence of shear-mediated ulcer formation. Trained professionals should perform skin and nail care in these individuals.

Ulcer treatment

The first step in the treatment of a patient with diabetes who has a foot ulcer is medical management of the systemic diabetes. Many of these individuals are malnourished due to chronic renal disease or chronic infection. Many are immunocompromised. Once the systemic condition of the patient is optimized, specific attention can be directed to the foot ulcer.

Ulcers can be neuropathic or ischemic. Neuropathic ulcers are caused by pressure or by shear forces. Once the ulcer is unroofed and the necrotic tissue is debrided, the soft tissue base reveals healthy granulation tissue. If the ulcer is unroofed and the tissue at the base is necrotic, the ulcer is likely to be ischemic. A vascular surgeon should evaluate patients with ischemic ulcers to determine if the limb can be salvaged. A risk-benefit analysis then can then be performed to determine whether treatment should entail limb salvage, amputation, or a combination of both. If the ulcer is neuropathic, noninvasive vascular testing is in order in the absence of palpable pedal pulses.

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.

Wet-to-dry wound care does not promote wound healing because dry wounds desiccate. This allows potential wound-healing cells to die and opportunistic infection to propagate. Keep dry wounds moist with saline-soaked dressings or hydrocolloid gels. Treat wounds that produce massive quantities of exudative material with absorbant materials (calcium alginate) and dressings while keeping the wound moist. Growth factor gels have been shown to promote wound healing in wounds with reasonable wound-healing potential.

Offloading distributes weightbearing pressure over a larger surface area and provides an interface to decrease shear forces. Elimination of weightbearing generally is not required. The optimal offloading device is the total contact cast (TCC). This device acts to dissipate weightbearing and shearing loads by eliminating foot or ankle motion, using an interface material to distribute pressure and shear forces. Venous swelling is lessened by the compression effect of the cast. When the ulcer shows appreciable improvement, foot care can be simplified with prefabricated walking braces that have a plantar weightbearing surface lined with Plastazote or other pressure-dissipating materials (see Image 3). When the swelling decreases or when ankle immobilization is not necessary, healing shoes can be used (see Image 4).

The grade 0 foot has no ulcers but is at risk. Treatment involves foot-specific patient education and appropriate footwear. Prefabricated pressure-dissipating insoles are appropriate. Occasionally, bony prominence or deformity (eg, bunion, hammertoe) cannot be accommodated by therapeutic footwear. In this situation, removal of the bony prominence (exostectomy) or correction of the deformity is advised to prevent ulceration. Increasing ulcer grade requires additional treatment. Grade I ulcers require debridement of nonviable or infected tissue, local wound care, and offloading. Grade II ulcers require debridement, culture-specific antibiotics, local wound care, and more extensive offloading techniques. Grade III ulcers require debridement of infected or gangrenous tissue. Partial foot amputation, more complex offloading or nonweightbearing, and culture-specific parenteral antibiotic therapy are necessary. Grade IV ulcers require partial or whole foot amputation.

Following wound healing, patients should use offloading permanently. The plantigrade foot can be managed with depth-inlay soft leather oxford laced shoes and custom accommodative foot orthoses. When plantigrade alignment cannot be obtained, an ankle-foot orthosis or surgical reconstruction or stabilization is required.

Persistent or recurrent ulceration

Ulcers that do not heal or that recur in appropriate footwear require careful evaluation. Heel impact or increased forefoot loading can be lessened with a cushioned heel and/or rocker sole modification of the shoe. Consider surgery when accommodative methods are unsuccessful. Increased forefoot loading or ankle equinus (static or dynamic) can be treated with percutaneous Achilles tendon lengthening followed by immobilization in a below-the-knee walking cast for 4-6 weeks. Plastic surgery intervention with rotational flaps or with free tissue transfer occasionally is indicated. The key to success in these patients is patient education, accommodative pedorthic footwear, and careful monitoring.

Prescription footwear

The Medicare Therapeutic Shoe Bill of 1993 provides financial support for 1 pair of appropriate inlay-depth shoes and 3 pairs of custom foot orthoses yearly for individuals with diabetes. Most insurance carriers have followed their lead with similar guidelines. They have realized that preventive strategies are cost-effective compared with amputation. The certified pedorthist is an essential consultant in providing these devices. The bill requires that both the physician treating the diabetes and the orthopedic surgeon or podiatrist treating the foot sign the prescription.

Charcot foot

Charcot foot is a hypertrophic osteoarthropathy currently seen primarily in patients with diabetes who have peripheral neuropathy. The etiology is neurotraumatic or neurovascular. The traumatic etiology implies fracture or stress fracture without protective sensation. The hypertrophic response is due to the inherent motion applied to a nonimmobilized fracture. The vascular etiology implies an abnormal vascular inflow, producing bony resorption, bony weakening, and a similar result. Eichenholtz stage I is the proliferative phase of the disease. The foot is very swollen. Radiographs are negative for fracture or dislocation. Stage II is the period of periarticular fracture or dislocation. Stage III is the phase of consolidation or healing.

Treatment historically has been anecdotal, with only recent attempts at a scientific approach. The foot with active disease is immobilized nonweightbearing in a TCC or other prefabricated device. When the process has consolidated, treatment has been accommodative, most recently with a specialized type of ankle-foot orthosis, the Charcot Restraint Orthotic Walker (CROW). Surgery is advised for bony infection, nonhealing ulcers, or deformity that cannot be accommodated with a custom orthosis. There is a recent trend toward attempted joint fusion in stages II and III, which is used to prevent deformity that will be difficult to accommodate with a shoe-orthotic construct.

Surgical therapy:
 

Amputation

Any discussion of the diabetic foot requires introduction of the concept of function-preserving amputation surgery. Partial and whole foot amputations frequently are necessary as treatment for infection or gangrene. The goal of treatment is preservation of function, not just preservation of tissue. Amputation surgery should be the first step in the rehabilitation of the patient. Because most of these individuals are ambulatory, direct surgical planning at creating a terminal end organ of load-bearing that can interface most easily with accommodative footwear, prosthesis, or a combination of both (ie, prosthosis). Employ the principles that direct construction of a residual limb for weightbearing with a prosthesis when performing debridement or partial foot amputation.

The major value of partial foot amputation is the potential for retention of plantar load-bearing tissues, which are uniquely capable of tolerating the forces involved in weightbearing. The soft tissue envelope should be capable of minimizing these forces. Avoid the use of split-thickness skin grafts in load-bearing areas. Deformity should be avoided as much as possible. Use tendo-Achilles lengthening to avoid equinus deformity and increased loading of the residual forefoot in partial foot amputations. Retention of a deformed foot with exposed bony prominence leads only to decreased walking ability and recurrent ulceration.