Diabetic Foot

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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).

FIGURE 85-1 Evaluating protective sensation with 5.07 Semmes-Weinstein monofilament.

Peripheral Vascular Disease

The metabolic end products of increased blood glucose can also cause damage to blood vessels. Advanced glycosylation end products can damage the vascular endothelium, leading to microthrombosis and capillary obstruction. They also increase low-density lipoproteins, which can lead to atherosclerosis. Diabetic patients are more than twice as likely as nondiabetic patients to develop peripheral arterial disease, and the condition is more severe in diabetics.

The ankle-brachial index can be unreliable for the diagnosis of peripheral arterial disease in diabetic patients, because calcification of arteries can lead to elevated results, masking the severity of the disease. Toe pressure or TcpO₂ is thought to be more reliable in diabetic patients (Fig. 85-2). Angiography is the gold standard for diagnosing arterial lesions that may require intervention; however, it may be complicated by the fact that many diabetics have renal disease, which can be worsened by the intravenous contrast medium used in such studies.

FIGURE 85-2 Measurement of toe systolic pressure with manual PPG unit (Smartdop 45, Hadeco Inc., Kawasaki, Japan).

(From Romanos MT, Raspovic A, Perrin BM: The reliability of toe systolic pressure and the toe brachial index in patients with diabetes, Foot Ankle Res 3:31, 2010.)

Delayed Bone Healing

Displaced lower extremity fractures, including those treated with open reduction and internal fixation, take longer to heal in diabetic patients. In animal studies, the biomechanical strength of fracture callus was lower in diabetic specimens and collagen synthesis was decreased. Diabetic rats have been shown to have decreased cellular proliferation at the fracture site and decreased mechanical stiffness. Treatment with insulin improved these parameters to those of nondiabetic rats.

Altered Immune Function

Defects in leukocyte response to infection include problems with cell chemotaxis, adherence, phagocytosis, and intracellular killing. Because of this altered immune function, diabetic patients have an 80% increased risk of cellulitis, a fourfold risk of osteomyelitis, and double the risk of sepsis and death from infection.

Known risk factors for diabetic foot complications as outlined by The American Foot and Ankle Society include peripheral neuropathy as tested with the 5.07 Semmes-Weinstein monofilament, signs and symptoms of vascular insufficiency including absent pulses, trophic skin changes and/or a history of claudication, partial or total foot amputation, previous ulcer, previous hospital admission for a diabetic foot infection, bony deformity, peripheral edema, and abnormal skin temperatures. Care of the diabetic foot may require multiple specialists, including an orthopaedic surgeon, vascular surgeon, endocrinologist, infectious disease consultant, and pedorthotist.

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.

Pathophysiology

Patients who develop ulcers usually have a combination of peripheral neuropathy, deformity or joint contracture, increased plantar pressure, and peripheral arterial disease. Because of the loss of sensation, patients do not realize that undue pressure is placing their skin at risk. Motor neuropathy can lead to deformity such as claw toes; the bony prominences from the deformity make the skin more vulnerable to breakdown (Fig. 85-3). Achilles contracture can lead to increased forefoot pressures, which increases the chances of forefoot ulceration. There are known structural changes in the Achilles tendon in diabetic patients, including disorganization of the tendon fibers and calcification within the tendon. These changes are more prevalent in older patients and can explain the increased stiffness that is known to occur in the Achilles tendons in diabetics. Peripheral arterial disease also places the skin at risk and leads to impairment of healing once ulceration does occur. The presence of peripheral arterial disease increases the risk of ulceration ninefold.

FIGURE 85-3 A and B, Fixed flexion deformities of interphalangeal joint of hallux and proximal interphalangeal joint of second toe on left foot. C, Neither first nor second metatarsophalangeal joint could be passively flexed to neutral.

The Wagner classification (Box 85-1) is the most commonly used for grading foot ulcers. The University of Texas San Antonio classification system adds the criteria of infection and ischemia and correlates more closely with prognosis because increased severity (higher grade) is associated with longer healing times and amputation.

Box 85-1

Wagner Classification for Foot Ulcers

Grade 0—skin at risk

Grade 1—superficial ulcer (Fig. 85-4)

Grade 2—exposed tendon and deep structures (Fig. 85-5)

Grade 3—deep ulcers with abscess or osteomyelitis (Fig. 85-6)

Grade 4—partial gangrene

Grade 5—more extensive gangrene

FIGURE 85-4 Superficial (Wagner grade I) ulcer.

FIGURE 85-5 Deep (Wagner grade 2) ulcer with exposed tendon and joint capsule.

(From Brodsky JW: The diabetic foot. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Elsevier.)

FIGURE 85-6 Wagner grade 3 ulcer (A) with underlying osteomyelitis (B).

(From Brodsky JW: The diabetic foot. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Elsevier.)

Treatment

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.

FIGURE 85-7 A, Plantar ulcer healed (B) after 2 months in total contact cast.

FIGURE 85-8 Technique for application of total contact cast. A, Stockinette applied and cut to eliminate wrinkles. B and C, Vertical felt strips placed down medial and lateral sides of leg and malleoli, and cast padding applied over them. D, Felt pad made for plantar surface; note radial cuts to aid contouring around heel. E and F, Self-adhesive foam placed over toes and trimmed. G and H, Casting tape applied over all layers.

(From Brodsky JW: The diabetic foot. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Elsevier.)

FIGURE 85-9 Metal stirrup applied to total contact cast takes pressure off plantar surface of foot and transmits it to shank of cast.

(From Tamir E, Daniels TR, Finestone A, Nof M: Off-loading of hindfoot and midfoot neuropathic ulcers using a fiberglass cast with a metal stirrup, Foot Ankle Int 28:1048, 2007.)

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.

FIGURE 85-10 Removable diabetic boot can be used as alternative to total contact cast. A, Exterior. B, Interior.

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.

FIGURE 85-11 Cellulitis, abscess, and osteomyelitis arising from ulcer over fifth toe caused by tight shoe.

(From Brodsky JW: The diabetic foot. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Elsevier.)

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).

FIGURE 85-12 A and B, Drift of toes to fill defect created by amputation of toe.

(From Brodsky JW: The diabetic foot. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Elsevier.)

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.

FIGURE 85-13 Grade 3 ulcer under second metatarsal head extends into metatarsal head with presumptive contiguous osteomyelitis.

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.

FIGURE 85-14 A, Hallux laceration related to loss of normal joint mobility; during weight bearing, clinical hallux rigidus places pressure at interphalangeal joint. B, Planned resection arthroplasty of first metatarsophalangeal joint. C, Ulcer healed in immediate postoperative period.

(From Frykbreg RG, Zgonis T, Armstrong DG, et al: Diabetic foot disorders: a clinical practice guideline [2006 revision], J Foot Ankle Surg 45[Suppl]:S1, 2006.)

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

Pathophysiology

The most plausible explanation for the development of neuropathic arthropathy in a diabetic foot is loss of autonomic control of the vasculature. Resting blood flow in patients with diabetic neuropathy may be five times normal values. Arteriovenous shunting also has been documented in these feet. This high flow rate results in osteopenia, and, combined with somatosensory loss of pain and proprioception, multiple small mechanical insults unrecognized by the patient and occurring in osteopenic bone set the stage for bony dissolution and loss of structural integrity, followed by a collapse deformity (Fig. 85-15). Even with minor trauma to the foot (sprains, contusions, minor fractures), neuropathic skeletal changes may develop in a patient with diabetes mellitus.

FIGURE 85-15 A and B, Collapse at Lisfranc joints, valgus posturing of forefoot, and shortening of first ray. Prominence medially is medial cuneiform. C, Same foot with subluxations at tarsometatarsal joints, fragmentation of bone, shortening and angulation of first ray, and new bone formation.

Evaluation

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.

FIGURE 85-16 A and B, Anteroposterior and lateral radiographs show destruction of tarsometatarsal joints. Note equinus deformity on lateral view. C and D, Technetium (R3) and indium scans strongly suggest osteomyelitis in addition to neuropathy.

Percutaneous bone biopsy has been recommended to differentiate Charcot arthropathy and osteomyelitis. In a recent study in which percutaneous bone biopsies were done in 41 diabetic patients in whom osteomyelitis was suspected, the authors concluded that approximately 25% of patients suspected to have osteomyelitis but who have a negative percutaneous bone biopsy will develop osteomyelitis.

Classification

Stages of Charcot arthropathy as originally described by Eichenholtz with modifications are:

Stage 0: No radiographic changes, marked warmth and swelling after injury.

Stage 1: Fragmentation. Erythema, warmth and swelling of the extremity, with subluxation/dislocation of joints and bony debris and fragmentation of subchondral bone.

Stage 2: Coalescence. Decreased erythema, warmth and swelling of the extremity, with absorption of fine debris, new bone formation, and coalescence of larger fragments.

Stage 3: Consolidation. Resolution of swelling; however, residual deformity is present, with remodeling of bone seen on radiographs.

The anatomical classification as described by Brodsky with modifications includes five types (Fig. 85-17):

Type 1: Involvement of the tarsometatarsal joints. This is the most common type and often leads to the rocker-bottom deformity and plantar ulcerations secondary to bony prominences in this area.

Type 2: Involvement of the Chopart and subtalar joints. The second most common affected area, type 2 involvement also can lead to a rocker-bottom deformity with plantar flexion of the talar head. Marked varus/valgus of the hindfoot also can develop.

Type 3A: Involvement of the ankle. Marked varus or valgus usually develops, with ulceration over the prominent malleoli. This rarely can be controlled without surgery because of the degree of deformity that develops.

Type 3B: Involvement of the calcaneus. This can be an avulsion of the posterior tuberosity of the calcaneus and can lead to ulceration of the overlying skin. Another type involves joint depression, which can result in varus or valgus deformity and flattening of the talar declination angle. A third type includes fracture of the anterior process of the calcaneus, which can lead to instability of the lateral column that causes instability of the talonavicular joint.

Type 4: Involvement of multiple regions.

Type 5: Involvement of the forefoot. This is a rare form, and dislocation of the metatarsophalangeal joint can lead to ulcerations over metatarsal heads.

FIGURE 85-17 Dorsal (A) and lateral (B) views showing anatomical classification of Charcot arthropathy (see text).

(Redrawn from Brodsky JW: The diabetic foot. In Coughlin MJ, Mann RA, Saltzman CL, editors: Surgery of the foot and ankle, ed 8, Philadelphia, 2007, Elsevier.)

Treatment

Nonoperative Treatment

Total contact casting with protected weight bearing is the usual treatment for Charcot arthropathy. Initially, the total contact cast should be changed weekly to accommodate the decreased swelling and prevent ulceration when the cast becomes loose fitting. The course of casting may take several months and can be minimized by patient compliance with protected weight bearing. Weight bearing can be progressed in a total contact cast when instability decreases and bony consolidation occurs. After casting, patients should be protected with custom orthotics or bracing.

Bisphosphonates may reduce bone turnover in Charcot arthropathy and help with pain relief. Calcitonin also has been shown to decrease in bone turnover. These pharmacological agents are rarely used.

Operative Treatment

Surgery is required for approximately 25% of patients with Charcot arthropathy. Goals of operative treatment include deformity correction and stabilization to create/maintain a braceable, infection-free foot and ankle. It can be considered limb salvage surgery, because it helps to avoid amputation.

Surgical treatment of Charcot arthropathy may be required for severe instability that cannot be controlled with immobilization without causing ulceration. It also may be necessary after consolidation if severe deformity causes recurrent ulceration. If infection occurs, surgery may also be required. Typically, surgery is done during the coalescence or consolidation phase, because fixation may be difficult in the osteopenic bone that is present in the fragmentation stage. Surgery during the fragmentation phase may be necessary, however, for severe instability or infection or for acute dislocation. A more aggressive approach is possible with the stronger fixation techniques that have become available.

Surgical procedures that may be used for Charcot arthropathy of the foot and ankle include exostectomy to remove bony prominences causing ulceration, open reduction and internal fixation of acute cases, arthrodesis for deformity and instability, débridement for infection, and amputation for severe infection or deformity. Before surgical intervention is considered, appropriate medical workup should be obtained, including a vascular surgery consultation to test for adequate blood flow for healing.

Exostectomy should be done only if it does not lead to further instability (Fig. 85-18). Incisions should be made away from the ulcer and should be full thickness down to bone, avoiding undermining of the superficial soft tissue. Appropriate removal of bone should be done without affecting stability, reattaching important tendons as needed. Achilles tendon lengthening often is necessary.

FIGURE 85-18 A, Incision for removal of plantar bony prominence. B, Chronic plantar ulcer in neuropathic foot resistant to conservative treatment. C, Radiograph shows plantar bony prominence (arrow). D and E, Mass is exposed circumferentially. F, Wound is closed with large sutures in single layer, closing dead space. Percutaneous lengthening of Achilles tendon frequently is needed. G, Twenty-one months after bony resection and use of protective insert and shoe.

Arthrodesis may be indicated for deformity correction and for instability. Stronger fixation may be required for patients with Charcot arthropathy because of the relatively osteopenic bone and/or because of the difficulty that many of these patients have with non–weight bearing and because of the poor healing potential. Postoperative immobilization should be longer than in other patients, and bracing after casting often is required. There is a high nonunion rate for arthrodesis in patients with Charcot arthropathy; however, because of the neuropathy the nonunion is asymptomatic and if stability is maintained, a nonunion may not require revision surgery. The use of bone stimulators can be helpful.

Amputation may be necessary as a last resort in the presence of severe infection, severe instability, or loss of bone stock that precludes adequate fixation (Fig. 85-19). As for all other surgical procedures, adequate medical and vascular workup should be done preoperatively to maximize healing.

FIGURE 85-19 A and B, Charcot arthropathy with severe infection and instability.

For Charcot arthropathy of the ankle, tibiotalocalcaneal arthrodesis with an intramedullary nail often is required to control the severe instability that occurs (see Chapter 11). Occasionally, talectomy may be required to correct deformity before arthrodesis. If talectomy is required, however, the postoperative complication rate is higher (Fig. 85-20).

FIGURE 85-20 A and B, Charcot arthropathy. C and D, After tibiotalocalcaneal arthrodesis with intramedullary nail.

Hybrid external fixation may be attempted for patients with Charcot arthropathy of the ankle and osteomyelitis to prevent amputations. Infected tissue should be débrided, followed by arthrodesis preparation and application of the fixator (Fig. 85-21). Intravenous antibiotics should be administered, and open wounds can be treated with negative pressure wound therapy to try to avoid the need for free flap coverage.

FIGURE 85-21 A and B, Charcot arthropathy of ankle with osteomyelitis. C, Clinical appearance of foot with medial ulcer. D and E, Removal of infected talus. F, Application of hybrid external fixator. G and H, Postoperative radiographs showing hybrid fixator in place.

Surgical treatment of hindfoot and midfoot arthropathy includes arthrodesis: triple arthrodesis for type 2 and midfoot fusion for type 1. Resection of wedges of bone may be necessary to obtain deformity correction, and bone grafting may be required to fill in gaps after deformity correction. Large screws (6.5 to 7.3 mm) should be used in the hindfoot, and a combination of plates and screws may be necessary in the midfoot. For the midfoot, placing a plate on the plantar surface of the bones takes advantage of the tension band principle and may provide stronger fixation (Fig. 85-22). Internal fixation for midfoot Charcot arthropathy can include a medial column screw, which is an 8.0-mm cannulated screw placed from the posterior talus into the first metatarsal (Fig. 85-23). Adjunctive fixation can be added for further stabilization. Achilles tendon lengthening is almost always needed, because most of these patients have an equinus contracture.

FIGURE 85-22 A, Charcot arthropathy of midfoot. B, Use of plate on plantar surface takes advantage of tension band principle to provide stronger fixation.

FIGURE 85-23 A and B, Midfoot arthrodesis with use of medial column screw.

(From Lusser R, Hintermann B: Midfoot arthrodesis in Charcot foot deformity with “Charcot screws.” In Pfeffer GB, Easley ME, Frey C, et al, editors: Operative techniques in foot and ankle surgery, Philadelphia, 2010, Elsevier.)

Patients at risk for complications from midfoot Charcot arthropathy include obese patients, those with severe bony deformity or a chronic ulcer with osteomyelitis, and those who are immunocompromised. Determining appropriate treatment for Charcot arthropathy of the midfoot first involves determining if the foot is plantigrade. If the foot is plantigrade, the patient can be treated with a weight-bearing total contact cast for 8 to 16 weeks, followed by commercially available extra-depth shoes and custom orthoses. If the foot is not plantigrade, surgical treatment is recommended. For a low-risk patient, this includes Achilles tendon lengthening, débridement of infected or nonviable tissue, deformity correction, and internal fixation. For poor surgical candidates, a thin-wire fixator can be used instead of internal fixation. Frames can be left on for 8 weeks, followed by total contact casting and therapeutic footwear. Platelet-rich concentrate and bone marrow aspirate can be used to augment the fusion. For forefoot Charcot arthropathy, if total contact casting has not been successful, treatment may include cheilectomy, resection arthroplasty, or arthrodesis (Fig. 85-24).