Confronting a dramatic situation: the charcot foot complicated by osteomyelitis.

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research-article2014

IJLXXX10.1177/1534734614545875The International Journal of Lower Extremity Wounds XX(X)Paola

Original Review

Confronting a Dramatic Situation: The Charcot Foot Complicated by Osteomyelitis

The International Journal of Lower Extremity Wounds 2014, Vol. 13(4) 247–262 © The Author(s) 2014 Reprints and permissions: sagepub.com/journalsPermissions.nav DOI: 10.1177/1534734614545875 ijl.sagepub.com

Luca Dalla Paola, MD1

Abstract Charcot osteoarthropathy is a serious complication of diabetic neuropathy. Its prevalence in the diabetic population varies in the literature in relation to certain variables, such as the method of assessment, clinical or instrumental; the population studied; and the scope of the selection. This article is intended as a review of the recent literature concerning Charcot osteoarthropathy in its evolution and complications characterized by the development of ulceration and subsequent bone infection. Diagnosis and treatment strategies—either medical or surgical—are discussed both for Charcot arthropathy and osteomyelitis. Keywords diabetic foot, Charcot osteoarthropathy, osteomyelitis, diabetic foot surgery Charcot osteoarthropathy involving the foot and the ankle is a progressive disease that causes progressive deformity and osteoarticular degeneration, which easily leads to severe morbidity for the patient, due to instability, frequent ulcerations, and, consequently, a high risk of amputation1-5 (Figures 1.1 and 1.2). In the literature, the prevalence of Charcot arthropathy diagnosed in the diabetic population varies from 0.08% to 7.5%.1,6 Such prevalence can increase up to 13% if one considers the populations of high-risk patients such as those referring to specialized centers for the treatment of diabetic foot.1,3 The lack of standardization of both clinical and radiological diagnostic criteria leads to a high degree of approximation in recognizing the prevalence of Charcot arthropathy. This is further complicated by the inexperience of many health professionals as far as this disease is concerned.7 In a study on 68 patients treated for a midfoot localization of Charcot arthropathy, Myerson et al noted that 25% of the patients they followed had not had a proper diagnosis before enrollment in the study. Initially, the diagnosis was osteomyelitis, gout, arthritis, fracture, venous insufficiency, or malignancy.8 Charcot arthropathy has an extremely negative impact in terms of disability, morbidity, and quality of life of the diabetic patients who suffer from this condition.9-15 Though it has been over 150 years since it was first described, Charcot arthropathy is a condition still difficult to identify and treat. With an exponential increase in diabetes worldwide, health care providers need to be aware of

Charcot arthropathy and its potential limb-threatening complications in the foot and ankle.16 The typical diabetes patient who develops Charcot foot has had diabetes for >10 years, is morbidly obese, and has many of the organ system comorbidities associated with long-standing diabetes. For this reason, these patients are at extremely high risk for complications related to the disease and to the surgical procedures.17-19

The Course and the Anatomical Classification of Charcot Arthropathy Early literature contributions concerning Charcot arthropathy lacked clinical findings that correlated with radiographic descriptions of the disease. In 1966, Eichenholtz published a landmark article based on radiographic appearance and its physiologic course.20 He described 3 separate, but linear stages: development, coalescent, and reconstructive stages. Shibata et al modified the staging system proposed by Eichenholtz and added an even earlier stage to that of development, characterized by the absence of injury or osteoarticular disorders21 (Table 1).

1

Diabetic Foot Department, Maria Cecilia Hospital, Cotignola, Italy

Corresponding Author: Luca Dalla Paola, Maria Cecilia Hospital, GVM Care & Research, Via Corriera 1, Cotignola 48010, Italy. Email: [email protected]

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Figure 1.2. Diabetic Charcot foot complicated by plantar midfoot ulceration: medial aspect of the foot.

Figure 1.1. Diabetic Charcot foot complicated by plantar midfoot ulceration.

Many authors have developed different anatomical classifications of Charcot arthropathy starting from the clinical observation of the patterns of destruction to the foot and ankle.4,6,22,23 In diabetic Charcot arthropathy, Sanders and Frykberg identified 5 patterns of destruction in the foot and ankle and correlated these different anatomical patterns with the frequency of onset: Pattern I (forefoot) 15%; Pattern II (tarsometatarsal joint) 40%; Pattern III (naviculocuneiform, talonavicular, and calcaneocuboid joints) 30%; Pattern IV (ankle and/or subtalar joint) 10%; Pattern V (calcaneus) 5%4,23 (Table 2). The most severe structural deformity and instability are found at the Lisfranc joint and at the ankle/subtalar joints. Destruction at the calcaneal level is not common but may be associated with an isolated pathologic fracture or avulsion injury of the posterior tuberosity.22 In 2007, Brodsky described an anatomical classification based on the 4 areas most commonly affected by Charcot arthropathy (Figure 2). Representing about 60% of the anatomical sites that develop Charcot arthropathy, type I (midfoot) is considered the most common site and includes the metatarsocuneiform and naviculocuneiform joints. These locations are often associated with symptomatic exostosis. The second most common

location, type 2 (hindfoot), involves the subtalar, talonavicular, or calcaneocuboid joint. In this location, the presence of exostoses is less common. Type 2 accounts for approximately 30% to 35% of all locations. Type 3 is subdivided into “A” and “B”, that is, ankle and posterior calcaneus, respectively. Approximately 9% of the clinical presentations of Charcot arthropathy are of type 3A, involving the tibiotalar joint and its associated bones. The least common location is type 3B, with 2% of the clinical manifestations being a pathologic fracture of the tuberosity of the calcaneus. Brodsky also noted that the breakdown of soft tissues from bony prominences occurred most commonly in the Type I pattern and that these ulcers were located on the plantar surface of the foot.22 Trepman et al highlighted the failure to include multiple locations at forefoot level, and therefore changed Brodsky’s anatomical classification.24 Because of the high percentage of involvement of the midfoot and medial column of the foot, these locations were further differentiated into an additional number of classes. Schon et al investigated a cohort of 109 patients, describing the various midfoot deformities.25 The “Lisfranc pattern” has radiographic breakdown involving the first 3 metatarsocuneiform joints, and as the stage progresses in severity from A to C, the fourth and the fifth metatarsocuboid joints become involved. The “naviculocuneiform pattern” is seen when the majority of radiographic deformities occur more proximally and medially at the naviculocuneiform joint. Less significant deformity may be detected in the central column and laterally at the level of the fourth and fifth metatarsocuneiform joint. The “perinavicular pattern” includes the navicular and its surrounding bones, and patients with this pattern may have a tendency toward an adducted forefoot. The “transverse tarsal pattern” involves significant deformity in the talonavicular joint, including the medial and central columns. It was also noted that the


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Dalla Paola et al Table 1. Evolution of Charcot Neuroarthropathy. Acute

Chronic

Stage 0

Stage 1

Swelling

Debris formation at articular margins Fragmentation of subchondral bone Erosion of articular cartilage Osteolysis and osteopenia

Local warmth Mild erythema Clinical instability Radiographic changes absent MRI: bone marrow edema and microfracture and cysts with more severe injury

Disorganization and fragmentation of bone Soft tissue edema Increased joint mobility Subluxation/dislocation Deformity

Stage 2 Lessening of edema Absorption of fine debris Healing of fractures Fusion and coalescence of larger fragments Loss of vascularity Sclerosis of bone Deformity

Stage 3 Further repair and remodeling of bone Fusion and rounding of large fragments Revascularization Diminution of sclerosis Restoration of stability Increased bone density Exuberant ossification Deformity

Table 2. Frykberg and Sanders Anatomic Classification. Pattern

Location

Description

I

Forefoot

II

Tarsometatarsal joints

III

Naviculocuneiform, talonavicular, and calcaneocuboid joints

IV

Ankle and subtalar joints

V

Calcaneus

Involving the IPJs, phalanges, MTP joints, and/or distal MT bones commonly occurring pattern, also seen with plantar ulceration; seen as osteopenia, osteolysis, juxtaarticular cortical bone defects, subluxation, and destruction on radiographs Involving the tarsometatarsal joints and metatarsal bases, cuneiforms and cuboid; commonly occurring pattern, with greater frequency in diabetic patients than in patients with leprosy; may be associated with plantar ulceration at the apex of deformity; seen as subluxation or fracture-dislocation, collapse of midfoot, and resultant rocker-bottom foot deformity on radiographs; may have dorsal prominence at metatarsal bases; late changes include fragmentation Involving usually the naviculocuneiform joint and navicular bone but also the other midtarsal joints and bones; ulceration may occur at the apex of deformity and may be in combination with pattern II; on radiographs, seen as osteolysis of naviculocuneiform joints with fragmentation; with osseous debris both dorsally and plantarly Involving the ankle joint with or without the subtalar joint an medial or lateral malleolar fracture; considered a severe structural deformity with instability—may even be associated with minor ankle sprain; on radiographs, seen as malleolar fractures, erosion of bone and cartilage with collapse of joint, free bodies in ankle, extensive destruction, and lateral dislocation of ankle Rarely involving only the calcaneus bone and usually involving an avulsion fracture of the posterior tubercle; although no joint is involved, the pattern develops in patients with Charcot foot; on radiographs, seen as osteolytic changes in the posterior calcaneus attachment of the Achilles tendon; avulsion fracture of the posterior tubercle may ensue

most severe “rocker-bottom” phase in any of the 4 patterns of Charcot midfoot could lead to ulceration and/or infection at the midfoot.25 The medial column of the Charcot foot was also further divided into 5 clinical stages using clinical parameters, radiographs, and bone scans.26

As in the modified Eichenholtz classification, the first stage is called stage 0, in which the medial column is hot, edematous, and often painful; in this phase, the X-ray examination is negative. The same symptoms are also found in stage 1, with radiological findings of periarticular cysts, erosions, and localized osteopenia. If dislocations


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Figure 2. Brodsky’s anatomic classification.

AP (A) and lateral (B) drawings demonstrating Brodsky’s anatomic classification of the Charcot foot. Type 1 involves the tarsometatarsal and naviculocueniform joints. Type 2 involves the subtalar and/or the Chopart joint. Type 3A involves the ankle joint. Type 3B involves fracture of the posterior calcaneal tuberosity. (Reproduced with permission from Brodsky JW: The diabetic foot, in Coughlin MJ, Mann RA, Saltzman CL, eds: Surgery of the Foot and Ankle, ed 8. St.Louis, MO, Mosby, 2006, p 1341.)

are detected, the disease is in stage 2, usually with anatomical involvement of the second metatarsocuneiform joint. Stage 3 is characterized by joint dislocation and collapse of the plantar arch, while stage 4 represents the healed stage with sclerotic fusion of the affected bones and joints. In the natural history of Charcot neuroarthropathy, the deformity and instability of the ankle follow the acute phase in which, despite the edema and the acute inflammatory components, a plantigrade foot position may still be maintained. With or without non-weightbearing therapy, the limb may develop joint dislocations, fractures, and deformities. Ankle instability associated with pronation or supination while walking contributes to the development of ulceration on the medial or lateral aspect of the midfoot, rearfoot, or ankle (Figure 3). The progression of infection is frequent. In these cases, the risk of major amputation is high.1,19,24,27,28 The acquired deformities are further complicated by large wounds overlying the bony deformity and underlying contiguous osteomyelitis. Once patients develop associated foot ulcers and chronic osteomyelitis, their risk of lower extremity amputation and premature death is significantly greater than in similar, nonaffected diabetic individuals.13,29,30 Callus and blister formation may be observed as a sequela of Charcot arthropathy.31 Ulceration is present in 43% of Charcot feet affected at midfoot level and in 53% of all Charcot patients.8,17 Concurrent ulceration, present in 40% to 44% of patients with acute Charcot arthropathy, may make it more difficult

Figure 3. Charcot foot with flail ankle.

to exclude the possibility of infection. The presence of a foot ulcer may necessitate further evaluation and treatment including hospital admission, non-weight-bearing,


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Dalla Paola et al empirical antibiotic coverage, and diagnostic imaging such as magnetic resonance imaging (MRI) or nuclear medicine scans. In a study in which 55 subjects with acute Charcot arthropathy were assessed, 4 patients (7%) developed a new-onset ulceration 10 months after returning to permanent footwear.32 In another group of 54 patients with Charcot feet, all 15 patients (28%) who developed ulceration in an area of bony prominence required the excision of the bony prominence to successfully heal the ulcer.33

Differential Diagnosis of Charcot Arthropathy and Osteomyelitis Charcot osteoarthropathy and osteomyelitis are difficult to diagnose when they occur concurrently, but it is important that differential diagnosis is included in the limb salvage plan. Differentiating between the 2 types is important because treatment varies greatly depending on the disease: Charcot arthropathy is treated differently from a Charcot foot associated with osteomyelitis or osteomyelitis alone. If an infection develops, regardless of the presence of Charcot osteoarthropathy, the osteomyelitis needs to be addressed and eradicated for successful treatment, which is accomplished in a staged strategy.

Diagnosis of Osteomyelitis Butalia et al recently published a meta-analysis to determine the sensitivity and specificity of the clinical history, the physical examination, the laboratory tests, and the plain radiographs in supporting the diagnosis of osteomyelitis in the diabetic foot. The conclusions of this study were that bone biopsy should be considered the “gold standard” for the diagnosis of osteomyelitis. The study also highlighted that lesions extending more than 2 cm2 and a positive probeto-bone test were the most relevant clinical findings for suspecting osteomyelitis, while from an instrumental standpoint an erythrocyte sedimentation rate of more than 70 mm/h increases the probability of diagnosis, and abnormal plain radiographs double the odds of diagnosis. The study concluded that no single historical feature or physical examination reliably excludes osteomyelitis.34 The probe-to-bone test is a clinical test that has been relied on over the past 14 years. In 1995, Grayson et al described it using a sterile blunt metal probe to determine if bone could be felt through an ulceration site. The results of the study showed a sensitivity of 66% in diagnosing osteomyelitis. They reported an 89% positive predictive value and a 56% negative predictive value. The conclusion drawn from the study was that if the ulcer probed to bone, more than likely it represented osteomyelitis and advanced imaging studies were unnecessary.35

More recently, Shone et al reported a positive predictive value of only 53% and a negative predictive value of 85%.36 In another recent large study conducted by Lavery et al on 1666 diabetic patients, the probe-to-bone test had a very low positive predictive value (57%) but a high negative predictive value (98%).37 Surgical percutaneous bone biopsy specimens after a 14-day antibiotic-free period represent the gold standard of care for the diabetic foot.38 The sensitivity and specificity have been reported at 95% and 99%, respectively.39 At histopathology signs of osteonecrosis can be observed, while at micropathological level one can identify both acute and chronic processes. An acute infection will have neutrophil infiltration, while chronic infection will show plasma cells and lymphocytes. When bone cultures are being obtained, it is recommended that antibiotics be withheld for at least 48 hours prior to culturing. Soft tissue pathogens may not always reflect the organism involved in the underlying osteomyelitis, mandating that both deep soft tissue and bone be sent for analysis.40 Ge et al found that 75% of wounds had multiple organisms with an average of 2.4 organisms per wound.41 For the diagnosis of osteomyelitis in Charcot foot, unlike osteomyelitis in simple neuropathic ulcer, a complex assessment with advanced radiological imaging is very often required instead of a clinical evaluation. This is due to the need to assess not only the presence but also the extent of the infectious process that often involves the bone structures of the midfoot and/or ankle. The imaging studies must be interpreted in conjunction with the clinical exam and the laboratory values, to assist in the diagnosis of osteomyelitis. Plain film radiography should be the first imaging modality to use. Although sensitivity and specificity of plain films are poor, they are easy to obtain and relatively inexpensive in comparison to other imaging techniques. Osteomyelitis appears as permeative radiolucencies, destructive changes, cortical defects, and/or periosteal new bone formation42 (Figure 4). The specificity of plain film radiography tends to be higher than its sensitivity, but can be compromised by nonspecific osseous reactions.43 Plain film radiographic signs of osteomyelitis may be lacking in the first few weeks, as it takes 30% to 50% bone loss before they become evident on radiographs. Bone scans with Technetium-99 methylene diphosphonate (Tc99m) detect changes in bone in a more timely fashion when compared to plain film radiographs. The sensitivity for this imaging modality using 3- or 4-phase scans approaches 90%, which is an improvement over plain film radiography.44 The specificity is much lower averaging less than 50% and is secondary to increased bone turnover in most bone disorders such as fractures, postoperative changes, and noninfected Charcot foot. Therefore, this technique is not


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Figure 6. MRI and T2 image of midfoot/ankle osteomyelitis.

Figure 4. Plain radiography with evidence of midfoot osteomyelitis.

Figure 5. MRI with T1 image and evidence of diffuse midfoot/ ankle osteomyelitis.

considered of great help in evaluating and screening for osteomyelitis in Charcot foot disease.44,45 MRI can aid in the diagnosis of diabetic osteomyelitis due to altered signal intensity of the affected bone. MRI is helpful in patients with surrounding soft tissue infection because it captures both soft tissue and bone. Sensitivity of MRI is reported between 90% and 100%, while specificity ranges between 80% and 100%.44 The normal high signal intensity of T1 images due to marrow fat in bone is replaced with decreased signal intensity, while the T2 image, which is typically darker in healthy bone, shows increased signal intensity (Figures 5 and 6). It is important to correlate MRI results with the clinical picture as well as the laboratory values. This will make it

easier to discriminate the findings that are consistent with the diagnosis of Charcot arthropathy from those related to the superimposed infection. Although costly, MRI provides for great anatomical detail and is a useful tool in operative planning. Kapoor et al recently conducted a meta-analysis on the usefulness of MRI in diagnosing foot osteomyelitis. Sixteen studies met the inclusion criteria in order to compare the performance of MRI versus bone scan, white blood cell scanning, and plain film radiography. MRI was shown to have a sensitivity of 90% and a specificity of 83%, with an overall accuracy of 89%. MRI was found to be superior to plain radiography, Tc bone scanning, and labeled white cell scans in the diagnosis of foot osteomyelitis.43 In a meta-analysis, Dihn et al found that MRI was the most accurate imaging test for the diagnosis of osteomyelitis.42 According to Dihn et al, both computed tomography and positron emission tomography have not been adequately tested in the diabetic population to recommend their use for the diagnosis of osteomyelitis.42

Antibiotic Therapy for Charcot Complicated by Osteomyelitis The underlying principle behind nonsurgical treatment is to administer antibiotics while providing a local environment in which the medication can work.46 The antibiotic treatment schedule for osteomyelitis in the diabetic foot and therefore also in Charcot arthropathy must consider factors such as the ability to penetrate the bone, the route of administration, and the duration of therapy. The length of treatment depends on whether the margins of surgical resection are free from infection. The antibiotic therapy should be selected based on the isolates obtained from culturing the infected bone. Recommendations for the medical treatment of osteomyelitis provide for parenteral antibiotic therapy for 6 weeks.47


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Dalla Paola et al Antibiotic therapy should be as targeted and as narrow spectrum as feasible, with the assistance of bone cultures when possible.48 In a population of 50 patients, Senneville et al found that bone culture based antibiotic therapy was the only variable associated with disease remission.49 Unfortunately, no antibiotic has proved to be superior in the eradication of osteomyelitis.46,48 It is imperative to always cover Staphylococcus due to its high prevalence, possibly also methicillin-resistant Staphylococcus following its isolation from a culture or due to local high prevalence based on epidemiology data. Game and Jeffcoate found that methicillin-resistant Staphylococcus aureus colonization was linked with prior hospitalization.50 There is no evidence that any particular route, either parental or oral, is either superior or inferior to the other.46-48 If highly bioavailable antibiotics are used, high antibiotic plasma levels can be achieved either with drugs administered parenterally or orally. Although the length of antibiotic therapy is frequently discussed in the literature, there is no hard data to guide decision making as to the duration of treatment. Four to 6 weeks of parenteral antibiotics are proposed in conjunction with surgical debridement for the eradication of osteomyelitis. More recently, some reports have highlighted that a shorter treatment with parenteral antibiotics in combination with a more prolonged oral antibiotic therapy is equally effective. Currently, there is no substantial scientific evidence that lays forth a protocol of medical therapy that gives a consistent, predictable result.51 Game and Jeffcoate reported on 113 diabetic patients treated nonsurgically with antibiotic therapy.50 Oral therapy was chosen for 80% of the patients, while 20% received parenteral therapy followed by oral antibiotics. The mean duration of therapy for oral treatment was 9 weeks, while the IV group had a mean duration of 2 weeks. Overall, 93 patients (82%) were in remission at 12 months. Embil et al treated diabetic osteomyelitis with oral therapy in 79 patients. Patients were treated with a mean of 3 oral antibiotics, for an average duration of 40 weeks. With this therapy, 80% of patients achieved remission with a mean relapse-free period of 50 weeks.52

Surgical Treatment of Charcot Osteoarthropathy Complicated by Osteomyelitis Surgical treatment has historically been limited to resection of infected bone, when life or limb were at risk, or simple resection of bony prominences that precluded the use of the cumbersome accommodative devices.53

Figure 7. Collinearity of the talus axis and first MTP joint axis.

Patients were treated with these accommodative methods until infection or severe deformity necessitated amputation. The use of standard orthopedic metallic foreign body implants is further precluded in over half of patients because of the presence of wounds overlying the deformity that are, at best, contaminated or, more likely, complicated by underlying osteomyelitis at the time of presentation.28,54,55 Even if foreign body implants are avoided, the extensive surgical dissection often used in correcting such a deformity would be at substantial risk of wound failure or infection. The factor that ultimately greatly reduces the possibility of surgical correction of the deformity is the poor biomechanical quality of the bone, which leads to failure of the surgical construct even after some time.56 Bevan et al found that patients who are radiographically consistently plantigrade are at low risk of developing ulcerations or infections.73 These authors studied the radiographs in weight-bearing conditions. They observed that if a line drawn through the axis of the talus (representing the axis of the hindfoot) was reasonably collinear with another one drawn through the axis of the first metatarsal (representing the axis of the forefoot) the risk of developing a lesion was indeed low (Figure 7). In order to describe the surgical management of Charcot arthropathy with osteomyelitis, one needs to define and introduce some general principles applied to the surgical treatment of infected ulcerated lesion complicated by osteomyelitis.


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Figure 8.2. Wide debridement of devitalized tissues: postoperative.

Figure 8.1. Wide debridement of devitalized tissues: preoperative.

Debridement is defined as the surgical removal of infected or necrotic tissue from below and/or around a wound with underlying osteomyelitis. Conservative surgery is defined as the removal of infected bone and surrounding soft tissues, while amputation is the removal of a portion of the foot. In turn, amputations can be subdivided into 2 categories: minor and major amputations. Minor amputations are amputations of a portion of the foot below the ankle joint, while amputations proximal to the ankle joint are known as major amputations. Depending on the degree of bone and soft tissue involvement, the surgeon will decide whether to perform debridement or amputation. Whether one treats an osteomyelitic focus with a surgical or nonsurgical approach, all infected ulcerations should be debrided with the drainage of any obvious purulence. Debridement of the wound aids in the healing process by converting a chronic wound to an acute wound as well as allowing the clinician to properly visualize the wound bed. Debridement also allows for the removal of devitalized tissue that helps reduce the area of a nidus for infection (Figures 8.1 and 8.2).

We usually recommend that such debridement is performed in the operating room, especially if it is to be extended proximally to the fingers and the mid-hindfoot. This allows for better pain control through appropriate anesthesiology techniques and good bleeding control. There are several indications for the surgical management of osteomyelitis. Patients who have failed medical antibiotic treatment or patients with evidence of abscess formation, necrotizing fasciitis, or gangrene should undergo surgical treatment. There are some key concepts that a surgeon must keep in mind when surgically treating a patient with osteomyelitis of the foot. The surgeon should debride to bleeding viable bone, resecting all infected and necrotic bone. Wide excision of bone with margins >5 mm has been shown to reduce the recurrence rate in chronic osteomyelitis as opposed to marginal or limited resection < 5 mm.57 Clinically infected surgical sites should be left open, and repeat debridements may be necessary.54,58-60 Once bleeding and clinically evident infectious components are under control, the use of negative pressure wound therapy may be appropriate (Figure 9). If the infected bone is resected along with all soft tissue involvement, primary closure is an option (Figures 10-12). Antibiotic-loaded bone cement may be beneficial in the face of infection and can aid in filling a dead space left by resection of tissue. If delayed primary closure is impossible, negative pressure wound therapy followed by the use of dermal substitutes and/or skin grafts or flaps could be scheduled.58


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Figure 11. Surgical site after bone resection.

Figure 9. Negative pressure wound therapy after surgical debridement.

Figure 12. Primary intention closure.

Figure 10. Preoperative lesion.

Following surgical debridement, culture-guided antibiotic therapy should be started and continued for 2 to 6 weeks. Ha Van et al reported on the contribution of conservative surgery versus nonsurgical management of diabetic foot osteomyelitis. One group was treated nonsurgically with offloading, antibiotic therapy, and wound care. The other

group was treated similarly with the addition of surgery, which was defined as the resection of a phalanx or metatarsal bone. The nonsurgical group had a healing rate of 57%, with a mean time of 462 days. The conservative surgical group showed a healing rate of 78% with an average of 181 days to wound closure. The number of secondary surgical procedures, which included amputation and revascularization, was significantly higher in the nonsurgical cohort. Also, the duration of antibiotic treatment was much higher in the nonsurgical group than in the surgical one (246 days vs 111 days).61 When formulating an algorithm for the treatment of Charcot arthropathy, it is essential to address all factors that will have an impact on outcome. In the treatment of Charcot foot complicated by osteomyelitis, the goal of therapy should be to control bone infection before final reconstruction. The process of reconstruction and stabilization of Charcot foot in the presence of an active ulcerative lesion require appropriate antibiotic treatment, resection of the


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lesion and the bone affected by the infectious process, exchange of bone cement or replacement of the defect with bone graft, or primary arthrodesis with external fixation. In these patients, negative pressure wound therapy and the use of dermal substitutes and/or skin grafting may be necessary.62 For maintaining the deformity correction achieved in reconstruction, Steinmann pins can be used for stabilization with compression by an Ilizarov external fixation device for midfoot, hindfoot, and/or ankle joint. Other options for surgical reconstruction include internal, external fixation, arthrodesis versus exostectomy, with the goal being complete fusion, although pseudoarthrosis can create a stable lower extremity allowing for ambulation and reduced risk of ulceration/re-ulceration. In a recent article, Aragon-Sanchez et al presented their experience in the treatment of patients with diabetic foot osteomyelitis where a conservative approach had been taken, defined as no amputation of any part of the foot. They analyzed the factors that determine the outcomes of surgical treatment of osteomyelitis of the foot in diabetic patients given early surgical treatment within 12 hours of admission and treated with prioritization of foot-sparing surgery and avoidance of amputation. They found that conservative surgery without local or high-level amputation is successful in almost half of the cases of diabetic foot osteomyelitis. The risks of failure in the case of conservative surgery were exposed bone, the presence of ischemia, and necrotizing soft tissue infection.63 The overall strategy for surgically managing a severe diabetic foot infection is infection control through aggressive and extensive surgical debridement, a comprehensive vascular assessment and subsequent revascularization by means of percutaneous angioplasty or bypass, and finally soft tissue and skeletal reconstruction after infection is eradicated to obtain wound closure and limb salvage. The first step in planning complex surgery for this disease is to lengthen the gastrocnemius-soleus muscle unit by either percutaneous lengthening of the tendon or fractional lengthening of the musculotendineous junction.28,54,55 The purpose of this treatment is to establish a muscle balance between the ankle flexor and extensor muscles. This makes it possible to correct the equinus bending moment due to a prevalence of the muscles of the posterior compartment and resulting motor imbalance at the junction between the hindfoot and the forefoot during midstance of gait. This bending moment may well be responsible for the location of the acquired deformity at the midfoot level in more than 85% of patients.17 The second step is excision of all soft tissue and bony structures involved in the infection (Figures 13-15). Bone biopsies should be sent to the laboratory for histopathologic and microbiological assessment.

Figure 13. Surgical approach to acute soft tissue and bone infection: lateral aspect.

Figure 14. Surgical approach to acute soft tissue and bone infection: medial aspect.

Figure 15. Exposition of deep soft tissues and bone infected.


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Figure 16. Talus dislocation.

Figure 17. Lateral approach to tibiotalar joint of the right ankle.

The culture isolates obtained from intraoperative bone biopsies should serve as a guide for parenteral antibiotic therapy. Even in the presence of negative cultures, patients with clinically infected lesions should undergo a course of parenteral antibiotic therapy. It was also noted that many of the patients with a lesion at the level of an exostosis had positive cultures obtained from the surgical removal of that portion of the bone. Also this “silent” bone infection should be treated with targeted antibiotic therapy. The third step is correction of the deformity to create both a clinically and radiographically plantigrade foot. This surgical step may be done at the same time of the previous approach to the osteomyelitic focus, but if there is major infectious involvement of the soft tissues, it may be postponed after resolution of the acute infection. Correction of the deformity is usually achieved through wedge osteotomy with resection of a wedge of bone. The treatment of osteotomy may range from simple tangential sequestrectomy to more complex procedures such as modified triple arthrodesis. If the bony structures of the hindfoot and/or ankle are also involved, bone resection must be performed in such a way as to reconcile 2 often conflicting needs, that is, the need to remove as much infected bone as possible and the need to maintain sufficient bony structures for fusion. The treatment options range from a simple wedge osteotomy of the heads of the subtalar joint and/or tibiotalar joint—thus obtaining a correction of the ankle varus or valgus deformity—to total talectomy with tibiocalcaneal fusion if, in the presence of subluxation or dislocation of the talus (Figure 16), there is evidence of complete infectious talar disruption62,64 (Figures 17 and 18). After correction of the deformity and soft tissue debridement one usually performs a primary intention closure. If there is too much flap tension and extensive debridement of

Figure 18. Infected talus removed surgically before tibiocalcanear fusion.

the infected tissues is performed, it is possible to use a closure by second intention. In this case, once bleeding is controlled, one can perform a course of negative pressure wound therapy with or without instillation of antimicrobial agents.62 Final coverage can be accomplished with the use of dermal substitutes and subsequent skin grafting (Figures 19.1 and 19.2). Reconstructive plastic surgery has occasionally been used after correction of the bony deformity. After correction of the deformity, foot and ankle immobilization/stabilization have to be warranted (fourth step) using a preconstructed circular external fixator.28,54,55,62,65-68 The Ilizarov method is used to create a stable clinical construct with the use of fine-tensioned wires and no implant at the site of the corrective surgery or previous infection (Figure 20).


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Figure 19.1. Application of dermal substitute on open surgical site: preoperative.

Figure 20. External circular frame.

Figure 19.2. Application of dermal substitute on open surgical site: postoperative.

The surgery employs limited surgical dissection and leaves no metallic foreign bodies at the site of surgery. The external fixator provides an extremely stable surgical construct during the healing phase without the use of bulky, encumbering casts. In 2012, Pinzur et al published a study conducted on the largest cohort of patients with Charcot arthropathy and osteomyelitis, in which he used a single-stage procedure for treatment. The first step of his protocol involved surgical eradication of the infection from the affected bone. Tissue cultures from the resected bone were used to guide parenteral antibiotic therapy. Sufficient bone was removed to allow correction of the deformity to a plantigrade position. Large smooth percutaneous pins were used for provisional fixation. Maintenance of the surgically obtained correction was achieved with a 3-level preconstructed static circular external fixator. Wounds were reapproximated when

possible and managed with dressings and wound care when they could not be closed. The circular external fixator was maintained for a period of 8 weeks in patients with deformity in the foot and a minimum of 12 weeks when the ankle was involved. Following removal of the external fixator, patients were managed in a weight-bearing total contact cast for 4 to 6 weeks, followed by a commercially available walker. Patients were transitioned to therapeutic footwear consisting of commercially available depth-inlay shoes and custom accommodative foot orthoses. Using this protocol, Pinzur was able to achieve 95.7% limb salvage with ambulation in commercially available therapeutic footwear.65 There have been several studies utilizing a similar protocol with high limb salvage rates for treating Charcot osteoarthropathy with osteomyelitis of the midfoot or the ankle. Farber et al reported on 11 patients with midfoot Charcot osteoarthropathy and ulceration, who underwent operative debridement, corrective osteotomy, external skeletal fixation, and culture-directed antibiotic therapy as a limb salvage procedure. Patients were transitioned from the external fixator to total contact cast, and all subsequently progressed to therapeutic footwear in 12 to 49 months of follow-up.66 In another study, 26 diabetic patients underwent surgical correction of nonplantigrade Charcot osteoarthropathy with midfoot deformity. Correction was obtained and maintained with a 3-level ring external fixator. Fourteen had infected


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Dalla Paola et al wounds complicated by osteomyelitis. Surgery included Achilles tendon lengthening, excision of infected bone, correction of the multiplanar deformity, and culture-specific parenteral antibiotic therapy. Twenty-four of 26 patients were ulcer- and infection-free and able to ambulate with commercially available depth-inlay shoes and custom accommodative foot orthoses.28 In another study, 8 patients with diffuse ankle osteomyelitis were treated by resection of all infected tissues and hybrid-frame compression arthrodesis. Fusion of 8 ankles and 4 subtalar joints was attempted. All patients received 6 weeks of IV antibiotics. Open wounds were treated with negative pressure wound therapy until closure was achieved. Frames were removed at 3 months and walking casts were applied for 1 to -2 further months. Ankle infection was eradicated in all patients. Seven out of 8 ankles fused at an average of 13.5 weeks. At an average 3.4-year follow-up, none of the 7 fused ankles required further surgery.67 In another prospective study, limb salvage through surgical treatment of midfoot or ankle osteomyelitis was evaluated. Out of 45 patients with Charcot osteoarthropathy and osteomyelitis who underwent debridement and attempted fusion with a 3-level ring external fixator, 39 patients healed using emergent surgery to drain an acute manifestation of the infection while maintaining the fixation for an average of 25.7 weeks.62 Pinzur et al presented a series of 49 feet with midfoot deformities that were followed for an average of 3.6 years. Twenty-six of the feet initially presented for care with open ulcers and/or chronic osteomyelitis. Treatment included debridement of the infected bone and surrounding soft tissues, exostectomy and partial excision of the deformed midfoot combined with bone stabilization, and attempted arthrodesis. All patients were managed postoperatively with long-term custom accommodative bracing. All but one of the patients remained ambulatory, and none required belowknee amputations.17 Patients with Charcot osteoarthropathy are extremely complex patients, with a series of comorbidities adding to the osteomyelitic complication. Treatment by a multidisciplinary team is an opportunity to optimize the care pathways, make rational use of the available resources, and achieve the best possible outcomes Pinzur et al conducted a study investigating the outcomes of a group of diabetic patients enrolled in a highly specialized center and being treated by a multidisciplinary team for Charcot arthropathy with osteomyelitis. While the overall observed-to-expected cost of care remained virtually unchanged, the positive impact of the model revealed an increased positive effect on patients with greater severity of illness and higher risk of mortality. The results of this study suggest that a proactive, cooperative, comanagement model for the perioperative treatment of high-risk patients undergoing complex surgery can improve the quality and

efficiency metrics associated with the delivery of service to patients.69

Conclusions The therapeutic plan for Charcot osteoarthropathy with concurrent osteomyelitis is extremely complex and very often lengthy. This is due to the need for a sequence of multiple surgical procedures, prolonged antibiotic therapy, extended periods of non-weight-bearing and immobilization, and use of specific technologies such as negative pressure wound therapy, engineered tissues, and external fixation. These therapeutic plans and protocols should be taken care of by multidisciplinary teams specifically trained on the subject. This is related to the extreme complexity of these patients and their increasingly serious comorbidities often involving the heart, the kidneys, and the brain. The treatment of Charcot osteoarthropathy complicated by infection and osteomyelitis is highly demanding—both physically and mentally—not only for the patient but also for the specialist. The patient should be aware of the extreme difficulty and length of such therapeutic plans and that there is no absolute guarantee of healing in the sense of freedom from infection and/or correction of the deformity nor an absolute elimination of the risk of recurrence. There are still some open issues regarding the duration of some components of the therapeutic plan (eg, antibiotic therapy and the period of immobilization). However, the biggest issue is still the comparison between reconstructive treatment and primary amputation. Probably this should be the goal of a comparative study to evaluate the pros and cons of limb salvage accomplished with reconstructive treatment versus below-knee amputation. From a health system perspective, patients with severe Charcot foot deformity and bony infection pose a notable drain on available health care resources. Once patients develop osteomyelitis, the decision-making algorithm becomes complicated. A significant percentage of these patients will require amputation, often after failed reconstruction attempts and multiple courses of antibiotic therapy.13 The first question that needs to be addressed is whether successful correction of the acquired deformity allows patients more independence. If the answer is yes, the following question would be: will this lead to a longer survival, compared with both the impaired quality of life associated with encumbered bracing and that of a transtibial amputee?10,70,71 Many experts currently believe that deformity correction in patients with Charcot arthropathy can potentially greatly improve their quality of life, foster greater walking independence, and improve longevity. Instead, detractors suggest that surgery is not justified given the cost of care and the risks associated with its complexity.


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Data from a recent study by Gil et al suggest that the cost of care for successful transtibial amputation may be very similar to the cost of limb salvage, at least during the first year.72 Mortality at 1 and 2 years following transtibial amputation is between 25% and 36% in the overall diabetic population.70,71 Another significant fact to consider is that these patients often have elevated body mass index and are unlikely to achieve independent ambulation following below-knee amputation and prosthetic limb fitting. Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding The author(s) received no financial support for the research, authorship, and/or publication of this article.

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