The neuropathic limb has autonomic, sensory, and motor components. Findings in autonomic neuropathy include loss of vasomotor, sweat, and sebaceous gland functions. These losses contribute to dry, nonelastic skin that can progress to xerosis and hyperkeratosis or skin that is atrophic and shiny with increased vulnerability to injury. Sensory neuropathy contributes to pathology in the neuropathic foot by delaying diagnosis because of lack of appreciation of pain from the wound. This tends to give the patient with sensory neuropathy a false sense of security that “nothing is wrong.” Although often not sufficiently emphasized, motor neuropathy also has profound consequences in the neuropathic foot. Motor neuropathy contributes to muscular atrophy, muscle imbalances, and deformities. These lead to abnormal concentration of forces and shear stresses, both of which are precursors to wound formation.
Bus et al.1 measured the cross-sectional area of intrinsic muscles of the feet in patients with diabetic polyneuropathy and control subjects without diabetes using magnetic resonance imaging. The goal of the study was to determine the associations among intrinsic muscle cross-sectional area, neuropathy, and the presence of claw and hammer toe deformities. They identified atrophy in the intrinsic muscle of subjects with neuropathy but not in the control subjects without diabetes. However, there were no significant changes in the metatarsophalangeal and interphalangeal joint angles, as would be expected to be present in patients with claw or hammer toe deformities. They concluded that intrinsic muscle atrophy is a common finding in patients with neuropathic feet but is not uniformly associated with toe deformities. Their conclusions must be considered in the context of a small sample size, absence of information about the duration of the neuropathy, and lack of information about findings in the long flexor and extensor muscles of the toes. Whereas atrophy and weakness may not lead to deformities, there is undoubtedly a high correlation between spasticity and muscle imbalances as a cause of these problems.
Bernstein2 observed that motor neuropathy typically progressed from the base of the first and fifth toes to the other toes. He labeled this phenomenon the “intrinsic minus foot.” As the muscles denervate, muscle imbalances develop between the flexors and extensors, causing flexion of the interphalangeal joints and hyperextension of the metacarpophalangeal (MTP) joints. This results in clawing of the toes. Hyperextension of the MTP joints depresses the metatarsal heads and with weightbearing pushes the metatarsal fat pads distally so they no longer provide cushioning over the bony prominences of the metatarsal heads. This causes pressure concentrations that lead to calluses, ulcerations, and infection. Atrophy of the intrinsic muscles of the foot was a frequent finding in Bernstein’s patient population. As the pathology progresses, extension of the MTP joints eventually causes upward rotation of the medial side of the forefoot (supination). The imbalance of the long extensor tendons to the toes leads to hyperextension of the MTP joints. Frequently, the long extensor tendons bowstring across the dorsum of the foot in association with the clawed hallux or “cock-up” hallux deformity. In summary, muscle imbalances lead to deformities. Deformities change the biomechanics of the feet and cause injuries to the soft tissues. Healing is delayed if loading of these structures continues because of repetitive stresses to the injured tissues.3
Andersen et al.4 assessed motor function in a comparative study of 34 noninsulin-dependent and 19 insulin-dependent patients with diabetes, using macroelectromyography and isokinetic dynamometry. They measured fiber density, the maximal isokinetic strength of the ankle and knee extensors, and the amplitude of the macro motor unit potential of the anterior tibial and lateral vastus muscles. All patients underwent a standardized clinical examination, including a neurological disability score and quantitative sensory examination. Motor nerve conduction studies also were performed. The amplitude of the macro motor unit potential and fiber density of the anterior tibial muscle were increased in patients with neuropathy without weakness (p < 0.05) and increased to a greater degree in patients with neuropathy and weakness (p < 0.05). The consequences of anterior tibial muscle weakness include: 1) foot drop resulting in foot slap in the early stance phase of the gait cycle; 2) toe drag in the late stance phase, resulting in callous formation over the tips of the toes; and 3) increased hip and knee flexion in the swing phase, characterizing the steppage gait.
Both the prevalence and severity of foot deformities are associated with increasing age. The risk of ulceration and lower extremity amputation is additionally increased when neuropathy is present. The presence of fixed deformities with associated pedal ulcers delays healing to a greater extent than does chronological age alone.3 Location of the deformity significantly influences healing times with total-contact casting. Average healing time for ulcers in the forefoot were 35 ± 12 days; midfoot, 73 ± 28 days; and hindfoot, 90 ± 12 days. The location of ulcers and location of fixed deformities on the neuropathic foot predicted healing times using total-contact casts.5 Delayed healing of hindfoot ulcerations probably is related to the extreme difficulty of off-loading the heel during the stance phase of the gait cycle. Wertsch et al.6 found that plantar loading was decreased only by 45% under the heel, as compared with 65% under the great toe, 63% under the fourth metatarsal, 69% under the first metatarsal, and 32% under the fifth metatarsal. The term “unloading” commonly used by orthotists refers to pressure relief, as opposed to pressure removal, which is termed off-loading or nonweightbearing. No orthosis is available that reduces the load on the heel sufficiently to promote healing yet allows gait activities.
Forefoot deformities present special problems for the fitting of footwear. Bunions, toe deformities, hallux abducto-valgus, and depressed metatarsal heads occur frequently in older adults who have associated weakness, poor endurance, postural instability, or combinations of these. If both insensitivity and foot deformities are present, footwear selection should be done with the help of a qualified footwear specialist.3 The realized benefits of properly fitted footwear include augmentation of wound healing and the prevention of recurrent and new wounds.
Postural instability, gait instability, and risk of falling are compounded when the individual has forefoot or digit amputations. However, fillers and rigid soles with or without rocker bottoms are effective in counteracting the potential problems that can arise when walking is resumed with these types of amputations. Diabetic sensory neuropathy causing inadequate sensory feedback affects the function of the stabilizing muscles that traverse the ankle joint. With loss of fine muscle balance, there is increased postural sway with walking and the generation of shear forces with loading.
Currently, nonoperative techniques to manage and prevent wounds in neuropathic feet focus on pressure relief, stabilization, and fillers. Specialized shoe wear must be approached from a hierarchical perspective. The first level of care is the off-the-shelf shoe that is custom sized to accommodate mild-to-moderate deformities and have space enough to allow the insertion of extra-depth padded inserts. The second level of footwear selection is the shoe with the above characteristics plus specific prescriptions, such as fillers, lifts, wedges, metatarsal bars, rocker bottoms, cut-outs, deformity-correcting straps, or combinations of these. Level three footwear consists of custom-designed shoes to accommodate major deformities. They likely will include many of the prescription items used for level two footwear. The final level of the footwear hierarchy is the Charcot restraint orthotic walker (CROW) boot, also termed a neuropathic walker. This custom-designed, user friendly (especially with regard to donning and removal) boot can accommodate the most severe and unstable foot and ankle deformities.
Although most neuropathic foot problems can be managed with nonoperative interventions, surgical interventions must be considered when problems persist or new, impending problems are developing because of deformities, muscle imbalances, or contractures. Proactive surgical procedures to reduce musculoskeletal deformities are practical, tested methods that complement footwear and off-loading strategies. Early surgical interventions can be time efficient and cost-effective managements.
When surgery is being considered for wounds, deformities, or both in neuropathic feet, wound oxygenation and the magnitude of the infection require equal attention to the wound itself. Deformities interfere with healing because of the mechanical problems they generate. Mechanical problems cause pressure concentrations or attenuation of soft tissues over the deformity, leading to callous formation, bursal formation, ulceration, and osteomyelitis. Frequently, patients with neuropathy-associated wounds do not realize they have a problem until they see stains on their socks or become aware of an unpleasant odor.
If the tissues are poorly oxygenated, the patient is at high risk for nonhealing or failed flaps and wound dehiscences after surgery. For wounds to heal and infections to be controlled, 20-fold or greater increases in blood flow and metabolic activity are required.6 If the examination, Doppler testing, or transcutaneous oxygen measurements indicate that these metabolic requirements are not likely to be met, vascular surgery consultation and angiography are indicated (see “Vascular Assessment of the Neuropathic Foot” in this issue). When oxygenation of tissues is inadequate, the use of hyperbaric oxygen therapy as an adjunct to wound perfusion may improve tissue oxygenation enough for wound healing to occur.7,8 In addition, properly selected wound dressing materials and optimal medical management are required for good outcomes with surgeries for problem wounds. Optimal medical management includes addressing the following conditions that have ramifications commonly associated with problem wounds in the neuropathic foot:
- Anemias, frequently in patients with diabetes and chronic wounds, especially in association with renal insufficiency.
- Malnutrition, especially with respect to adequate protein intake.
- Edema control with attention to fluid retention, chronic venous insufficiency, third spacing of fluids, or contraction of the fluid volume.
- Cardiac function deficiencies.
- Challenging wound flora that may require antibiotic combinations and special monitoring for optimizing dosing and avoiding toxicity.
- Diabetes care with careful control of blood glucose levels.
Most surgeries for managing wounds associated with the neuropathic, diabetic foot can be categorized into five types: 1) management of the ulcer, 2) correction of deformities, 3) wound closures, 4) amputations, and 5) procedures for special problems. Each has in-office, in-clinic, on-the-ward and in-the-operating-room counterparts. In-office management of the ulcers includes debridements with scalpels, forceps, scissors, curettes, or rongeurs. The advantage of such debridements is they can be repeated frequently with repeated clinic visits because the wound demarks healthy from unhealthy tissue. In contrast, there is a strong incentive to establish “surgical margins” with in-operating-room debridement, with the result that more tissue is sacrificed than would occur with the in-office approach. The two types of in-operating-room debridement are: excision of ulcers and debridement of underlying bone, cicatrix, and bursa; and saucerization, a procedure that involves surgically excising the entire wound base to remove scar tissue and unroof cortical bone to encourage the development of a new healthy granulation tissue base to form. With the establishment of healthy margins, primary closures may be done with reasonable expectations of uncomplicated healing.
In-office correction of deformities is done with joint manipulations and tenotomies for toe deformities. Patients should be instructed in joint manipulations and stretching to be done on a daily basis to maintain corrections or improve the contractures. Claw and hammer toe deformities are expediently managed in the office with percutaneous tenotomies of the bowstrung tendons and manipulations of the contracted joints to straighten the toes. The in-the-operating-room counterparts of these procedures are Achilles tendon lengthenings (preferably done percutaneously) and correction of deformities by ostectomies and osteotomies by minimally invasive techniques. An example of such is scoring of the metatarsal neck with a Kirschner wire through a single puncture wound in the skin and performing an osteoclasis through the scored bone to redirect and off-load the metatarsal head overlying a malperforans (diabetic) ulcer.9
Although wound closures are not usually considered to be in-operating-room procedures, there are office counterparts. These include skin closures with sutures or staples and partial approximations of wound edges with widely spaced sutures. This latter technique is particularly useful for reducing the surface area of the wound and can be done repeatedly as the viscoelasticity of the skin gradually accommodates to the tension of the partially approximating sutures. In the operating room, closures or coverage of wounds can be done with various surgical techniques. From more simple to more complex, they include split-thickness skin grafts, full-thickness skin grafts, rotation flaps, advancement flaps, microvascular free flaps, and combinations of these. When wounds cannot be covered or closed completely in the operating room, a small portion may be left open to heal by secondary intention. Occasionally the application of negative pressure wound therapy (e.g., The V.A.C. [Vacuum Assisted Closure], KCI International, Inc., San Antonio, TX) may be useful, especially for cavitary wounds, for promoting wound contraction and assisting with the removal of secretions.
Simple amputations such as partial and complete toe removals can be done appropriately in an office setting. By excising skin and joint capsule, the diseased toe can be removed with minimal difficulty. A rongeur can shorten and contour any protruding bone. In general, such amputations are left open to heal by secondary intention or with partially approximating sutures. When formal amputations are indicated, an operating room is required. Two goals should be met: adequate resection to achieve a primary tension-free closure, and preservation of as much tissue, especially underlying bony support, as possible. Thus, creativity and unconventional amputations may be needed for the neuropathic foot, such as ray resections, compound amputations in which half the foot is amputated at the forefoot level and the other half at the midfoot level, unconventional flaps such as using the skin of the dorsum of the foot to achieve plantar coverage, subtotal medial and lateral column resections, and very proximal midfoot amputations. The more proximal the amputation, the more consideration should be given to lengthening the Achilles tendon and temporarily stabilizing the ankle joint with a percutaneous pin. Naturally, the more unconventional the amputation, the more important the shoe wear prescription. Many foot amputation surgeries involve patients who have already had distal foot bypasses. One should exercise caution in shoe wear fitting any patient with a known distal leg bypass. High-topped shoes or leg braces requiring tight elastic stabilizing bands could compromise the bypass.
Procedures for special problems include toenail management in the in-office setting and management of Charcot deformities in the operating room. No patient with a neuropathic foot condition should leave the foot surgeon’s office with long, dystrophic, dysmorphic, or fungus-infected toenails. The primary goal for the management of Charcot arthropathy is accommodative shoe wear, up to and including the CROW boot. Superficial ulcers associated with Charcot arthropathy of the foot usually are successfully managed with bumpectomies and primary closures. When the Charcot arthropathy is “end stage” (a lower limb amputation has been recommended), complex surgical reconstruction, including massive debridement, realignment with or without osteotomies, and temporary stabilization with external fixation, is an option in the strongly motivated, highly compliant patient. A year’s postoperative care and convalescence is usually required for this management.
In summary, most surgical procedures for the diabetic foot can be done with minimal expenditures of time and equipment; that is, they can be done with minimally invasive techniques. The management of almost all wound problems of the neuropathic foot have in-office and in-the-operating-room counterparts. Successful, durable outcomes of surgery, particularly in this group of patients, require a team approach to postoperative management, including the primary care physician, medical specialists, and diabetic educators. Even more important to prevent recurrences or the development of new wound problems is patient compliance and family support. Finally, appropriate shoe wear prescribed by the prosthetist or orthotist is the final common denominator for allowing the patient to resume functional ambulation without undue risk of developing new or recurrent wound problems.
1. At what stage in peripheral neuropathy would surgical intervention reduce the deformities and functional deficits associated with progressive neuropathy?
2. How would candidates be selected for a surgical correction to prevent deformities?
3. Would surgical intervention be a cost-effective method for preventing deformities?
1.Bus SA, Yang QX, Wang JH, et al. Intrinsic muscle atrophy and toe deformity in the diabetic neuropathic foot: a magnetic resonance imaging study. Diabetes Care
2.Bernstein RK. Physical signs of the intrinsic minus foot. Diabetes Care
3.Sinacore DR, Muller MJ. Pedal ulcers in older adults with diabetes mellitus. Top Geriatr Rehabil
4.Andersen H, Stalberg E, Gjerstad MD, Jakobsen J. Association of muscle strength and electrophysiological measures of reinnervation in diabetic neuropathy. Muscle Nerve
5.Sinacore DR. Healing times of diabetic ulcers in the presence of fixed deformities of the foot using total contact casting. Foot Ankle Int
6.Wertsch JJ, Frank FL, Zhu H, et al. Plantar pressures with total contact casting. J Rehabil Res Dev
7.Strauss MB. Diabetic foot and leg wounds: principles, management and prevention. Primary Care Reports
8.Strauss MB, Bryant BJ, Hart GB. Transcutaneous oxygen measurements under hyperbaric oxygen conditions as a predictor for healing of problem wounds. Foot Ankle Int
9.Strauss MB. Orthopaedic surgeon's role in the treatment and prevention of diabetic foot wounds. Foot Ankle Int