Surgical Management of the Diabetic Foot

Diabetes and Lesions of the Foot
Diabetes is a common condition in the United States, affecting more than 10 million adults.¹ Wounds of the foot are the most common reason for hospitalization in patients with diabetes;^2,3 it is estimated that 15% to 20% of patients with diabetes will develop an ulcer on their foot at some point,⁴ and for many of these cases, the most appropriate treatment results in some form of surgery.
The foot is highly specialized to cope with a large degree of repetitive stress. Fatty tissue on the plantar surface and a thickened dermis and epidermis cushion and absorb repeated forces of compression, torsion, and shear during locomotion and standing. However, the pathophysiology of diabetes can significantly alter the wound healing process, leading to an increased risk for foot ulceration. McNeely et al⁵ found that a transcutaneous oxygen tension (TcPO₂) of less than 30 mmHg, absence of the Achilles’ tendon reflex, and foot insensitivity are 3 factors that are strong predictors of ulceration.
A simple test for sensation involves pressing a nylon monofilament against the skin to the point of buckling.⁶ Patients who cannot feel the monofilament are at particular risk for ulceration. In patients without sensation, the likelihood for ulceration is 9.9 times higher and the likelihood of amputation is 17 times higher than in patients who can feel the monofilament.⁷
The pathogenesis of ulceration is complex and involves the interaction of angiopathy, neuropathy, and immunopathy. Briefly, vascular impairment has been found to correlate with the development of diabetic foot ulcers,⁸ probably through ischemic skin changes leading to ulceration. There is debate about the precise role of angiopathy in the microvasculature, but it is likely that thickening of the capillary basement membrane impairs the flow of nutrients and possibly white blood cell migration, yet there is no evidence of impairment of oxygen diffusion.⁹
Neuropathy is the most significant risk factor for diabetic foot ulcers and is present in over 80% of patients with diabetes and foot lesions.^10–12 All aspects of nerve function including the motor fibers to the intrinsic muscles of the foot are affected. With the loss of function, the toes become drawn up into a claw-foot position, creating points of increased pressure or friction beneath the metatarsophalangeal joints, over the dorsum of the toes or at the tip of the toes. Autonomic dysfunction also results in the shunting of blood through direct arteriole-venule passages, reducing the extent of tissue perfusion.^13,14 The decreased awareness of sensation and nerve-induced deformity predispose the diabetic foot to ulceration by causing imbalances in the tendons that shift the load-bearing areas to unprotected parts of the plantar surface. In the absence of a neuro-inflammatory response, infection may occur without the patient being alerted by the usual clinical signs of inflammation.
Although there does not appear to be any significant impairment of humoral immunity in diabetes, at the cellular level, impaired leukocyte function¹⁵ and intracellular killing have been noted^16–18 and these can be partly or completely reversed with improved diabetic control. Cell-mediated immune responses are also impaired by elevated glucose levels.¹⁹

Charcot Neuroarthropathy
A further risk factor for foot ulceration in the diabetic patient is the presence of Charcot neuroarthropathy. While the cause of the condition is not completely certain, the most commonly accepted theory is that a neurovascular dysfunction results in destruction of bone and joints. The theory is that a neurally stimulated vascular response results in bone resorption and eventually joint collapse.¹⁰
In the early stage, there is an acute inflammatory process with fragmentation and destruction of the bone, visible on x-ray, and the foot is warm, red, and swollen. In the following phase, the Charcot joint appears to heal and x-rays typically show new bone formation and coalescence of the fractures. This is followed by long-term deformity of the joint.

Preventive Strategies
The risk of injury to the diabetic foot is high, and the consequences of injury can be severe, therefore prevention is undoubtedly the best strategy. Tight glycemic control is essential but many problems can also be avoided by strict attention to foot hygiene and to the use of well-fitting footwear. Injury or infection may be overlooked in the early stages due to the difficulty some patients experience in inspecting their feet, as well as the effects of poor eyesight and reduced perception of pain. The role of the clinician in detecting these problems is of particular importance.
Offloading is a term used to describe the elimination of abnormal pressure points in order to prevent the development or recurrence of foot ulcers or to promote healing. Ideally, offloading will reduce the pressure at the ulcer site while maintaining mobility. Specially designed footwear, walking sticks, orthotic walkers, and crutches all assist in reducing pressure at danger points, and total contact plaster casts (TCCs) are effective in the treatment of ulceration of the plantar surface.^20,21 The TCC is minimally padded, moulded to the shape of the leg, and is fitted with a heel for walking. TCCs distribute pressure evenly across the plantar surface of the foot and eliminate excessive concentrations of pressure at individual points.²²
Normally, plantar pressure is greatest in the forefoot, but when fitted with a TCC, a large proportion of the pressure is redistributed along the cast wall and to the rearfoot. Additionally, TCCs may control edema and help protect the foot from infection,²³ but another important aspect may also be that they “force” compliance more effectively than removable contact walkers (RCW) or half-shoes. For these reasons, Armstrong et al²² suggest that TCCs may be more effective at bringing about healing than other offloading devices.
Once all nonsurgical therapeutic options have been attended to, preventive surgery should be considered as a means of correcting deformities and minimizing the development of ulcerations, which may lead to much more drastic interventional surgery at a later date. Many ulcerations and complications of infection can be avoided or minimized if surgery is carried out in a timely fashion to improve vascularity, or to reduce mechanical trauma to the foot, wound, or plantar surface.^24,25

Preventive Surgery for Patients With Diabetes
Vascular surgery. As adequate tissue perfusion is necessary for the healing and delivery of antibiotics, the surgeon should determine the extent of ischemia and assess whether the risks of any proposed procedure will be justified by the functional benefit offered to the patient. The extent of claudication is not necessarily a useful indicator in patients with diabetes as neuropathy may mask the symptoms. It may be more useful to confirm a diagnosis of ischemia with Doppler systolic pressure measurements, Doppler ankle pressure measurements, and the ankle-brachial index, TcPO₂ monitoring, pulse volume recording and toe pressure measurements.
The options for treatment of vascular disease include percutaneous transluminal angioplasty (with or without stenting), revascularization with a bypass graft, or amputation to provide function and protective sensation in the remaining part of the foot or leg. Amputation may be necessary when there is overwhelming infection that threatens the patient’s life, when rest pain cannot be controlled or when extensive necrosis has destroyed large areas of the foot and lower leg. Although there may be multiple occlusions in the vessels supplying the foot, treating the most important lesion may improve blood flow sufficiently to promote healing of a lesion.
Podiatric surgery. A particularly useful role of surgery in the management of the diabetic foot is to intervene at an early stage to correct deformities in order to relieve pressure areas and to reduce the risk of developing an ulcer. To this end, tenotomy and exostectomy are commonly carried out and more rarely, claw-toe corrections and arthrodesis.¹⁹ Amputation may be considered preventive if the aim is to prevent systemic spread of infection. Criteria for amputation include sepsis, pain, and progressive gangrene.
Achilles tendon tenotomy. Percutaneous tenotomy may be used to correct a tight Achilles tendon that is causing flexible equinus deformity in the foot.²⁶ The technique usually only requires local anesthesia, which is infiltrated along the Achilles tendon. A sharp #11 blade is inserted through the skin and the tendon is severed. Postoperatively, patients will usually need to be in a cast for almost 6 weeks to prevent recurrence. This procedure has been shown to reduce forefoot pressures in patients with diabetes who have suffered with recurrent ulcers underneath the metatarsal heads.²⁶ The author has had excellent clinical results with percutaneous tenotomy and immediate ambulation in a postoperative shoe precluding the need for casting.
Exostectomy. Charcot neuroarthropathy is responsible for some of the most deformed and unstable feet. Charcot joint disease affecting the mid-foot causes dislocation of the bones and collapse of the arch, producing altered structure and focal points of increased pressure. Patients with intertarsal Charcot fractures may develop a “rocker bottom deformity”—a bony prominence on the plantar surface, which can lead to ulceration. Initially, these can be treated with offloading devices but occasionally the prominence is too large to allow offloading and surgery must be considered. If the joint is stable, simple exostectomy may be all that is required. However, significant instability may require fusion of the joints.
The procedure is carried out through a medial or lateral incision; a plantar incision should only be used if there is no alternative approach. While sufficient bone must be removed to eliminate the prominence, enough must be left behind to maintain stability of the joint. Postoperatively, immobilization with a cast is usually required for 6 to 8 weeks.

Hammer and Mallet Toe Correction
Diabetic neuropathy gives rise to an imbalance in the intrinsic and extrinsic muscles of the foot with the result that most patients with diabetes will develop fixed claw- or hammer-toe deformities. Typically there is plantarflexion deformity of the proximal metaphalangeal joint (hammer toe) or the distal interphalangeal joint (mallet toe).²⁷ There is a tendency for the second toe to be most affected, and less commonly, the third.^28,29
The affected toe projects distally to the other toes and the deformity may be so great that it is difficult to correct with custom-made shoes. In such cases, the patient is at risk for developing recurrent ulcers over the dorsal aspect, the proximal phalangeal joints, or plantar ulcerations under the affected metatarsal heads. Conservative treatment often leads to on-going problems of re-ulceration, while corrective surgery can bring about rapid healing and allow the patient to dispense with extra-depth shoes and orthotic devices.
Although surgery is effective at correcting these deformities, the risk of vascular insufficiency is high. Pre-operatively the vascular status of the affected toes should be assessed and the patient must be alerted to the risk of amputation of the toe if blood supply is lost.
Flexor tenotomy can be performed via an open or closed technique. An open technique is preferred if the patient still has sensation in the foot, as a closed technique may result in accidental interruption of the nerve supply. A transverse incision is made on the plantar toe surface at the proximal phalanx, the flexor digitorum longus and brevis tendons are then separated from the neurovascular bundle and severed.³⁰
Additionally, it can be helpful to resect bone and fuse the proximal interphalangeal joint that corrects the extension of the toe on the metatarsal head, and the flexion at the proximal interphalangeal joint. The correction can be held with a small pin inserted through the tip of the toe, which is removed after 4 to 6 weeks.¹⁹
The alternative percutaneous procedure provides excellent outcomes with minimal complications in patients with insensate feet where nerve bundles have already been compromised.²⁷ After local anesthesia (if needed) via digital block or toe injection, a target incision is made between the plantar creases of the metatarsophalangeal and proximal interphalangeal joints at the paramedical aspect of the toe. A #15 scalpel blade is positioned perpendicularly to the skin with the cutting edge facing the toe tip. The stab incision is carried as far as the bone, then the blade tip is slid between the flexor digitorum longus, the brevis tendons, and the bone. The scalpel is turned counter-clockwise to rupture the tendons and the toe is stretched to a normal position. Sustained firm stretching of the toe may be necessary if the joint capsules are fibrotic. The stab wound typically heals in a normal fashion, does not require primary closure, and the patient is able to mobilize immediately.

Arthrodesis
Arthrodesis of the tarsal-metatarsal area is used rarely to treat severe deformity or instability arising from a Charcot deformity of the mid- or hind-foot that is so great that special shoes cannot be made to accommodate the deformity.^31,32
There are many complications and technical difficulties involved in this operation. The goal of surgery is to reduce the deformity, hold the reduction, and achieve bony union. However, as the bones are usually soft and fragmented complete reduction is difficult to achieve. Rigid internal fixation with screws and plates can be used, but poor bone quality makes this difficult to achieve.^33,34 An alternative is to carry out internal fixation with autologous bone grafts.³⁵ Postoperatively, patients need to be immobilized for months until bony or fibrous union can be detected on radiograph.
External fixation may be used where the condition of the bone is too poor to allow internal stabilization. Using percutaneous techniques and external fixation frames, the surgeon can adjust and manipulate the Charcot foot after surgery and enable the patient to return to early weight-bearing.³⁶

Amputation
While the primary objective of preventive surgery in the patient with diabetes is to limit the development of ulceration and infection, the surgeon should aim to achieve this while preserving the maximum amount of foot function. Occasionally, amputation is the only remaining option to avoid the development of life-threatening sepsis. Partial foot amputation, if possible, is preferable to below-knee amputation. The most commonly performed partial foot amputations are ray amputation, transmetatarsal amputation, Chopart amputation, or Symes amputation.^37,38
Toe amputation. The level of infection and viable skin should dictate the level of amputation. The aim should be to salvage the maximum amount of proximal toe, up to the base of the proximal phalanx. If the capsule of the metatarsophalangeal joint must be entered, then the amputation should be taken to the neck of the metatarsal to avoid exposure of the articular cartilage. The wound may be closed with primary intention and drainage but with no skin tension, or may be allowed to granulate under a dressing while awaiting application of a split-thickness skin graft.
The surgeon should aim to preserve the attachment of the flexor hallucis brevis into the proximal phalanx if the big toe is to be amputated and if the level of infection permits, as stability is considerably enhanced. Amputated toes may be resected individually at the metatarsal necks or at the base of the metatarsals. These amputations only require a foam insert into the shoe to allow ambulation.
Ray amputation. A ray amputation is necessary if necrosis has spread through the base of the toes. An amputation more proximal than the metatarsal neck may be necessary to allow adequate soft-tissue coverage of the bone. However, removal of the metatarsal alters the weight distribution of the forefoot, increasing the risk for development of lesions under the remaining metatarsals. Ray resection should generally only be performed for a single outer ray (first or fifth). Removal of more than 1 ray leaves a narrow foot, which is difficult to accommodate in shoes and does not perform as well as a foot that has undergone a more extensive mid-foot amputation.³⁹
Mid-foot amputation. Mid-foot amputation is carried out at the proximal transmetatarsal level, or tarsal-metatarsal level if there is inadequate soft tissue to create an envelope. The bone cuts in the former should be through the proximal metaphysic of each metatarsal.⁴⁰ Patients may develop pressure ulcers under the remaining metatarsal shafts if the procedure is carried out more distally. To avoid the possible development of equinus and varus, the Achilles tendon can be lengthened percutaneously via 3 hemisection cuts. Postoperatively, toe fillers can be used in standard shoes to aid walking.
An alternative to the transmetatarsal amputation is the panmetatarsal head resection. Giurini et al⁴¹ suggest that this procedure may be more appropriate in certain patients as it avoids many of the structural and biomechanical pitfalls of the transmetatarsal amputation.
Major amputation. The negative consequences of high-level amputation are well documented. Leg amputation has an adverse effect on the remaining limb, as heel strike force and total contact time are both increased.⁴² This is reflected in the high incidence of ablative surgery on the contralateral limb, which can reach 50% within 2 years.^43–45
Patients function better with lower levels of amputation. Ninety per cent of patients with partial foot amputations will use prosthesis and remain mobile, compared to 75% of patients with below-knee amputations, with only 25% of patients with above-knee amputations.⁴⁶ The subsequent natural history for the patient with a high-level amputation is quite poor: various studies have reported a 5-year mortality rate of 40% to 70%.⁴⁵ This can be partly attributed to changes in the patient’s lifestyle, which becomes much more sedentary and restricted, adversely affecting overall health. Therefore, all efforts should be made to carry out the lowest-level amputation possible so that the patient can walk with or without prosthesis.

Symes, Lisfranc, and Chopart Procedures
The Symes procedure involves disarticulation of the ankle to retain the end weight-bearing surface of the distal tibia and the adipose weight-bearing tissue of the heel pad. The surgery is carried out in 1 or 2 stages separated by 6 to 8 weeks.⁴⁷ When done in 2 stages, the first stage requires the ankle to be disarticulated, while retaining the articular surface of the distal tibia and the soft tissue blood supply from the posterior tibial artery. In the second stage, the malleoli, and distal tibial and fibular flares are excised leaving a squared off residual limb that can easily be fitted with a prosthesis.⁴⁸
The Lisfranc procedure is an amputation proximal to the transmetatarsal level. It can result in considerable problems for the patient during walking, as there is a loss of support and push-off. However, the principle complication is a tendency toward equinus deformity from the loss of dorsiflexor attachments, which if severe, may require repeat amputation at a higher level. The Chopart amputation is also a forefoot/midfoot procedure, which suffers from the same gait disturbances as the Lisfranc procedure, and may make the patient prone to a more severe equinus deformity. Heel cord tenotomize can prevent this problem and is used by the author routinely.
High-level amputation. In an effort to preserve length as far as possible, it may be desirable to perform a high-level amputation in stages, with an initial operation to control the infection and later procedures to achieve wound closure.

Surgical Management of Ulceration and Infection
Despite all attempts at prevention, every year thousands of patients with diabetes will develop foot ulceration ranging from simple cellulitis through ulcer and abscess to osteomyelitis and gangrene. Surgery is often the quickest and most appropriate intervention, even in cases of cellulitis. Early and aggressive staged surgical intervention is usually indicated.
Acute infection. Although acute infection can result from any laceration or abrasion, in patients with diabetes, acute infection tends to arise at the nail plates or the inter-digital web spaces.⁴⁹
Acute cellulitis usually begins in the web spaces, and spreads along the tendons and lumbricals of each toe leading to deep space infection if left untreated. Ulcers of the heel usually arise in bedridden patients or from puncture wounds. Although ulcers are readily treated in the early stages, deep space infections and gangrene are responsible for the highest rate of major limb amputation.⁵⁰
Systemic signs and symptoms of infection such as fever, malaise, nausea, and ketoacidosis characterize deep space infections. They generally involve only the central compartment of the foot, but bacterial spread can occur from the central to lateral or medial compartments. Bacteria can spread to the dorsum of the foot following destruction of the interosseous fascia, and can then migrate along the flexor tendons to infect the calf and lower leg. Small vessel thrombosis gives rise to progressive tissue ischemia and necrosis, and continued inflammation brings about edema, a rise in deep compartment pressures, and eventual ischemic necrosis of the foot muscles.
Treatment of acute infection. Mild to moderate foot infections should be treated with rest, elevation of the foot to decrease edema, broad-spectrum antibiotics, and local tissue debridement to reduce the bacterial burden. Debridement is the removal of foreign matter and necrotic tissue from a wound.⁵¹ Edmonds⁵² gave the following rationale for debridement of ulcers: debridement enables the true dimensions of the ulcer to be perceived, and allows drainage of exudate and removal of dead tissue, both of which reduce the risk for infection. Debridement enables deep swabs to be taken for culture and encourages healing by restoring a chronic wound to an acute wound.
There is little evidence to support the role of debridement. Its widespread use is largely based on consensus opinion of experts rather than randomized clinical trials. Most clinicians favor the use of debridement and although currently there is no solid evidence, Moss et al⁵³ have shown debridement to be the first and most important step in healing. The removal of dead and contaminated tissue by excision of the wound margins and removal of senescent fibroblast cells is essential. The author uses aggressive, serial debridement.⁵⁴ Multiple debridements are often necessary. The Versajet^™ Hydrosurgery System (Smith & Nephew, Largo, Fla) allows a narrower excision.⁵⁵ As conversion of the chronic problem wound to an acute wound is rapidly performed with less trauma and minimal marginal tissue excised, even in the face of peripheral vascular disease.
Regular debridement can improve healing rates through the elimination of necrotic and infected tissue.⁵¹Staphylococcus aureus and facultative streptococci are the most common pathogens isolated in non limb-threatening infections⁸ and patients with acute localized cellulitis, without any accompanying neurotrophic ulcer, respond well to a 2-week course of outpatient antibiotic therapy: further surgery may be required.⁵⁶
Debridement may be carried out on an outpatient basis with the aim of removing all dead and contaminated soft and bony tissue. An off weight-bearing incision should be made whenever possible. These are painful, slow healing, and limit the mobility of the patient for a longer period. Generally, infections of the main compartments or the heel should be made on the medial or lateral aspects of the foot. Infections of the web spaces can be drained through diamond-shaped windows on the plantar surface and the dorsal aspect if the infection has extended dorsally. Incisions in the inter-digital part of the web space should be avoided, if possible, as they heal more slowly. Dorsal abscesses can be drained by incisions on the dorsal surface.
Heel ulcers often progress rapidly leading to osteomyelitis of the calcaneus if left untreated. Surgery, if possible, must be attempted from medial or lateral incisions, as incisions on the plantar surface will heal slowly—increasing the period of immobilization. Partial calcanectomy with or without primary closure may be necessary if osteomyelitis is present.
Following thorough debridement and drainage there are a number of options for wound closure including grafting, flaps, and advanced dressings. Options that have proven effective in the treatment of diabetic ulcers are the use of human skin equivalents (HSE) such as Apligraf^® (Organogenesis Inc, Canton, Mass), platelet-derived growth factor-BB (Regranex Gel^™, Johnson & Johnson, Somerville, NJ), and human fibroblast-derived dermal substitute (Dermagraft^®, Advanced BioHealing, La Jolla, Calif). Apligraf is a bilayered living-skin construct made up of an outer layer of keratinocytes and a lower layer of live allogenic fibroblasts on type I collagen dispersed in a dermal layer matrix. These are appropriate treatments for chronic ulcers as they add cells and growth factors to a wound environment that is deficient in these elements. Apligraf plus compression therapy has been found to be nearly 3 times more effective at achieving 100% closure than patients treated with compression alone.⁵⁷

Chronic Infection
Progressive claw-toe deformity leads to increased plantar pressure on the metatarsal heads.¹⁹ If offloading or preventive surgery are not carried out to interrupt the process, a circular neurotrophic ulcer develops on the callus, most commonly over the first, second, and fifth metatarsal heads. These ulcers can be deep with significant undermining of the margin, and tissue loss extending to the metatarsal head. Debridement may need to be extensive, including tendons and joint capsules. Infection of the deep compartment space may occur if a sinus tract develops between the ulcer and the deep compartment. This is demonstrated by the ability to express purulent foul-smelling liquid from the ulcer.
Limb-threatening foot infections are usually polymicrobial.⁵⁸ Although the precise composition reflects the patient’s local environment; the most common organisms are gram-positive cocci (S aureus, Group D and B streptococci), enteric aerobic gram-negative rods (E coli, Klebsiella, Enterobacter aerogenes, Proteus mirabilis, P aeruginosa), and anaerobes (B fragilis, Peptostreptococci, Clostridia spp). There is medical literature to suggest that S aureus is the most virulent pathogenic organism when isolated or as a component of a mixed infection. Deep tissue specimens are required to confirm the diagnosis but should not delay empirical antibiotic therapy. Various antibiotic regimens have been proposed for empirical treatment,^58,59 but a recent systematic review⁶⁰ found that there was insufficient evidence to recommend any particular antimicrobial agent for the treatment of diabetic foot ulcer.
Osteomyelitis. Chronic ulceration of the foot often leads to osteomyelitis, through the spread of contiguous soft-tissue infection to underlying bone. Accurate diagnosis is crucial, as osteomyelitis requires longer antibiotic therapy than soft tissue infection (4 to 6 weeks versus 7 to 14 days), and will possibly require surgical debridement to remove necrotic tissue. More importantly, delay in diagnosis may increase the risk for amputation. Osteomyelitis may not, however, be clinically obvious.⁶¹ In one study, 68% of patients with biopsy-proven osteomyelitis had no evidence of bony exposure in the wound.⁶² The main difficulty in diagnosing osteomyelitis in a diabetic patient lies in distinguishing bone infection from noninfectious neuropathic bony lesions, such as changes caused by Charcot’s disease, osteoporosis, and osteolysis. The characteristics of osteomyelitis are patchy bone destruction, with periosteal reaction and ill-defined bone margins.⁶³ However, none of the radiographical methods are sufficiently characteristic to distinguish unambiguously osteopathy from osteomyelitis. Sensitivity can be up to 100% but specificity may be no more than 69%.⁶⁴ There is a high chance of obtaining false negative results in the early stages.
Lipsky et al⁶⁴ reviewed the evidence for the various methods available for diagnosing osteomyelitis. The 3-phase bone scan (technetium-99, methylene bisphosphonate, and gallium-67 citrate) is relatively sensitive but may produce false-negatives particularly if blood flow is impaired. This technique may also produce false-positives and is probably most helpful in indicating osteomyelitis before radiographic changes are evident. MRI provides useful information about abnormalities of the bone and soft tissue, but does not clearly distinguish infection from other causes of bone disease.
Positron emission tomography (PET) imaging using F-18 fluorodeoxyglucose is emerging as an excellent noninvasive technique to diagnose osteomyelitis. Although false positive results can be caused by inflammation in the bone or surrounding tissue, overall PET scanning has been found to have a sensitivity of 100% and a specificity of nearly 90%.⁶⁵
The most accurate means of diagnosing osteomyelitis is through a biopsy of infected bone;⁶⁶ however, it requires highly precise sampling to ensure that an infected site is sampled and to avoid infected soft tissue and ulcers. In addition, patients receiving antibiotics may produce false-negative cultures.
Should a diagnosis of osteomyelitis be suspected, particularly in the presence of a soft-tissue infection, surgical debridement should be carried out on the abscess, callus, or ulcer to remove necrotic tissue and to determine the extent of infection. A specimen of bone can be taken for histology and culture and ideally treatment would be based on the culture results. However, broad-spectrum antibiotic therapy should be started immediately—this is the therapy expressly used by the author.
Treatment of chronic infection. In the absence of osteomyelitis, a 10- to 14-day period of antibiotics will usually be adequate while a more extensive therapy course of 4 to 6 weeks is usually required in the presence of osteomyelitis.
Ulcers with necrotic debris or local infection will require extensive surgical debridement, possibly including the plantar fascia, flexor tendons, volar plate of the metatarsophalangeal joint, and the head of the metatarsal bone. Infections extending into the deep spaces of the foot require a longitudinal incision along the plantar surface to provide adequate drainage and debridement. Intact vascular structures and viable muscle should be preserved, but tendons may need to be debrided, as they are more prone to undergo necrosis. In all cases, debridement should be taken back to healthy bleeding tissue.

Conclusion
The combination of angiopathy, immunopathy, and neuropathy substantially increase the risk that patients with diabetes will develop lesions of the foot and that they will be unaware of the problem until it reaches an advanced stage. Many patients with diabetes avoid seeking treatment and fear surgery, as it is associated with amputation. In reality, preventive surgery carried out at an early stage can be used to reduce focal points of pressure and to correct deformities that may increase the risk for ulceration and the need for more extensive surgery at a later date. A simple surgical procedure may also be the quickest and most effective treatment option if ulceration does occur. However, patients with diabetes are highly unlikely to request corrective surgery and it is the duty of all clinicians involved in their care to be aware of the possible benefits of early surgical intervention.