Charcot Foot

OrthopaedicsOne Articles

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16 Charcot foot

Contents

IntroductionPathophysiologyImpact on Health Related Quality of LifeClinical PresentationDiagnosisTreatmentConclusionsOther ImagesReferences

16.1 IntroductionIn spite of the massive amount of health system resource consumption directly attributed to diabetic footmorbidity, a 1999 editorial noted that only 3% of 6,661 clinical trials on diabetes-relatedDiabetic Medicineissues were concerned with diabetic foot morbidity. The goal of this review is to provide the reader asummary of our current understanding of the disease process named after the famous French neurologist,Jean Martin Charcot, and provide evidence-supported guidance for clinical management.

In 1868, Jean-Martin Charcot provided the first in-depth description of a destructive hypertrophicosteoarthropathy that affected joints of patients with tertiary syphilis. Penicillin has virtuallyeradicated tertiary syphilis, while insulin has allowed patients with diabetes to survive and develop thelongstanding peripheral neuropathy that appears to be the precursor for the development of a neuropathic(Charcot) osteoarthropathy.

Our modern understanding of neuropathic (Charcot) arthopathy is based on a benchmark monographpublished by Eichenholtz in 1966. He summarized the available literature and cataloged clinical,radiographic, and pathologic data in 68 consecutive patients. His light microscopy photographs demonstratethe pronounced osteoclastic activity that provides the basis of recent bone turnover and electron microscopyinvestigations. Based on his clinical and pathologic observations, Eichenholtz proposed a timeline of thedisease that was divided into three stages:

, initiation of the processStage I (Stage of Development), the active period of the disease process when bony destructionStage II (Stage of Coalescence)

and deformity occur, commencing when the destructive process burns out and theStage III (Stage of Reconstruction)

bone consolidates (heals) with the resulting deformity, making the patient prone for the developmentof tissue failure, deep infection and the frequent necessity for lower extremity amputation


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16.2 PathophysiologyThe development of peripheral neuropathy in individuals with diabetes is attributed to a complex interactionof glycosylated hemoglobin with arterioles of both central and peripheral nerves. The resultant progressiveloss of function is first appreciated in the smallest nerve fibers, leading to conduction defects in sensory,motor, and autonomic nerves. Precipitation of glycosylated hemoglobin at the arteriolar level is likelyresponsible for many of the co-morbidities associated with diabetes.

While there are more sensitive methods for detecting the presence of peripheral neuropathy, the acceptedclinical tool is the Semmes-Weinstein 5.07 monofilament (Figure 1). The lack of perception of 10 grams ofpressure (pressure applied by 5.07 monofilament) is considered the clinical threshold to support a diagnosisof diabetic peripheral neuropathy. This level of sensory neuropathy is present in approximately25% of adults with diabetes, as determined by population screening. While not universally true, mostpatients who develop Charcot foot arthropathy have this threshold level of peripheral neuropathy.

Semmes-Weinstein 5.07 monofilamentFigure 1.

Acute or sub-acute repetitive trauma is likely a key initiating event of the pathologic process that leads toCharcot foot arthropathy. The suggests that the inciting event is trauma. Without theneurotraumatic theorypresence of protective sensation, the patient continues to bear weight, eventually leading to a clinicalscenerio that mimics a hypertrophic non-union. The is predicated on anneurovascular theoryautonomic peripheral neuropathy that creates a high-flow vascular state in affected patients. This increasedblood flow simplistically washes out structural calcium from the bone, leading to localized osteopenia andmechanically induced deformity associated with continued weight-bearing. The truth is likely acombination of both theories.

Our current understanding of the effect of glycosylated hemoglobin on arterioles within central and peripheralnerves, leading to neuropathy, creates an excellent foundation for explaining the pathologic process. Someinciting event, likely trauma, initiates the production of the bioactive cytokines IL-1, beta IL-6, and TNF-alpha,which, in turn, activate osteoclastic recruitment, proliferation, and differentiation, thus initiating thedestructive process described by Eichenholtz. Baumhauer identified the specific cytokines and demonstratedthe presence of both an increased number of osteoclasts in affected tissue and increased destructiveosteoclastic activity. This concept is well supported by Gough, who demonstrated similar findings ofincreased unbalanced osteoclastic bone turnover based on measurement of serum and urine markers.


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The motor neuropathy, which initially affects smaller nerves and muscles, leads to a motor imbalance inwhich the larger and stronger foot and ankle plantar-flexor muscles overpower the smaller dorsiflexors.Recent evidence from several authors has clearly demonstrated increased static stiffness within the Achillestendon and the posterior ankle ligamentous tissues. This creates an intuitive pathomechanism to explain theinitiation of the destructive process. The motor imbalance created by the motor neuropathy applies anincreased bending moment during terminal stance phase of gait that apparently overloads the structures atthe midfoot level. The resultant forces appear to be responsible for upregulating the cytokines that turn onthe osteoclastic activity demonstrated pathologically and clinically.

16.3 Impact on Health Related Quality of LifeThe incidence of Charcot foot appears to be approximately 0.3% per year, based on a longitudinalobservational study of 3,000 Scandinavian patients with diabetes. Major complications related to thedeformity occur in 4% of patients. One hundred patients with Charcot foot arthropathy were followedfor 3 years as the target population used in validation of the AOFAS Diabetic Foot questionnaire. Thisinvestigation demonstrated a significant negative health related quality of life impact on affected patients.This negative impact was sustained, and not resolved following even successful treatment. Similarobservations were made from a small cohort of patients being treated in a specialty diabetic foot clinic, usingthe Short Musculoskeletal Assessment questionnaire (SMFA).

16.4 Clinical PresentationPatients typically present in the sixth or seventh decade. The vast majority were diagnosed with diabetes(both Types I and II) many years earlier. Most have clinical evidence of peripheral neuropathy, as measuredby insensitivity to the Semmes-Weinstein 5.07 (10 gm) monofilament. Occasionally, patients with neuropathyof other etiologies, such as alcohol, chemotherapy, and heavy metal, will present for treatment. Mostpatients are morbidly obese. Better than half of patients can cite a specific traumatic episode, often trivial,that initiated the process.

Patients classically were thought to present with painless swelling of affected joints. In fact, many patientshave pain associated with the swelling and deformity. While the involved foot is warm, swollen, anderythematous, the patient has an absence of clinical signs of sepsis, such as fever, leuccocytosis, elevatedblood sugar, or increased insulin requirement. A further clinical differentiation from infection can be made bylimb elevation. The erythema will decrease with elevation associated with arthropathy, as opposed toinfection. Patients with infection generally have some element of purulent drainage. Patients with Charcotarthropathy have drainage only if there is secondary infection of a pressure ulcer.

16.5 Diagnosis


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While multiple imaging techniques have been studied, the diagnosis is generally made clinically, andsupported with plain radiographs. The initial presentation is often confused with deep infection becauseaffected patients are generally poor hosts. While several diagnostic imaging techniques have shownpromise in differentiating acute neuropathic arthropathy from infection, none has been sufficiently specific towarrant routine use. Most patients are morbidly obese, have had diabetes for more than 10 years, andhave evidence of peripheral neuropathy as measured by insensitivity to the Semmes-Weinstein 5.07 (10 gm)monofilament. Several radiographic classifications have been developed based on anatomic locationand deformity; however, most experts use the original time-line advocated by Eichenholtz.

16.6 TreatmentBased on the notion that increased osteoclastic/bone turnover is the root cause of the disease process, theparenteral bisphosphonate pamidronate has been demonstrated to decrease bone turnover and clinicalsymptoms for a limited study period. While many clinicians have used oral bisphosphonates withunpublished anecdotal success, this form of treatment has not been approved for use by the US Food andDrug Administration.

16.6.1 Eichenholtz Stage I DiseaseTotal Contact Cast vs. Early ArthrodesisUp until the mid 1990s, Charcot arthropathy was thought to be a rare condition associated with any loss ofprotective sensation. Experts recognized it as a destructive process, and advised immobilization and theavoidance of further trauma by avoiding weight-bearing until the acute process resolved.

The non-weight-bearing total contact cast, which had become popular as a treatment for diabetic foot ulcers,was the accepted treatment standard for acute Charcot foot arthropathy. This approach was supported byseveral uncontrolled retrospective case series. There is approximately a 3% risk for the developmentof iatrogenic cast-associated ulcers, which generally resolve with local wound care and cast change.

The gold standard treatment of immobilization of the foot with a non-weight-bearing total contact cast untilthe foot was sufficiently stable to afford longitudinal management with accommodative bracing, was basedon expert opinion and confirmed by retrospective case series that had no historical or benchmark standardsor a recognized description of a favorable outcome. Two retrospective case series demonstrated similarresults when patients were treated with a weight-bearing total contact cast, changed at 2-weekintervals. Several retrospective case series supported the role of surgery for deep infection withsepsis, osteomyelitis, or when the resultant deformities subjectively could not be managed withaccommodative bracing.

Based on clinical observations that agreed with the more recently reported health-related quality of lifeoutcomes questionnaires, several investigators began to advise early surgical stabilization/arthrodesis withrigid internal fixation to avoid late deformity and/or the need for cumbersome accommodative bracing.Successful results were based on successful arthrodesis and limb salvage. No mention was made ofhealth-related quality of life or functional impact of disease.


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A retrospective review of patients managed in a Diabetic Foot clinic revealed that patients with a non-linearlateral talar--first metatarsal axis, as determined from weight bearing AP radiographs, were more likely todevelop late foot ulcers than those patients with a co-linear hindfoot-forefoot axis. When thisradiographic measure was combined with a clinical assessment of plantigrade vs. non-plantigrade weightbearing, it was retrospectively demonstrated that patients who were clinically plantigrade and possessed acolinear hindfoot-forefoot axis on weight bearing radiographs, could achieve the specific outcome ofmaintaining walking independence with longitudinal management with commercially-available depth-inlayshoes and custom accommodative foot orthoses.

16.6.2 Eichenholtz Stage II and III DiseaseAccommodative Bracing vs. Correction of DeformityCurrently, we do not have universally accepted definition of a "favorable outcome" that would allowcomparison between accommodative bracing and correction of deformity.

,Experts who advocate longitudinal management with accommodative bracing techniquessuch as custom-fabricated therapeutic footwear, accommodative ankle foot orthoses (AFO), or thecustom-fabricated Charcot Restraint Orthotic Walker (CROW), define favorable outcomes simplybased on limb preservation and the avoidance new ulcers or infections. As such, the reports areretrospective case series without benchmark controls.

advocate early arthrodesis forExperts who wish to avoid the use of accommodative orthosesacute (Stage I) disease and correction of deformity for later (Stage II and III) disease. They perceivethe accommodative orthoses as cumbersome and not well tolerated by their patients. They suggestthat correction of deformity and the provision of a stable foot allows the use of commercially availabletherapeutic footwear. Without benchmark controls, they define their surgical outcomes based onsuccessful arthrodesis or correction of deformity. Their case series also fail to report on the perceivedpositive impact on health related quality of life.

It is well accepted that patients with long-standing diabetes who have peripheral neuropathy, morbid obesity,and, often, severe localized osteoporosis are frequently poor surgical candidates. These characteristics putthem at high risk for mechanical loss of fixation with attempted surgical correction, as well as wound infectionor failure with extensive dissection. These observations have led many investigators to report onnon-controlled case series of patients treated surgically with correction of deformity and the maintenancewith fine wire ring external fixation in those patients arbitrarily defined as high risk for infection or mechanicalfailure.

Partial foot and Symes ankle disarticulation amputations have been discussed in retrospective case seriesas a functional alternative to other forms of treatment.

16.6.3 Ankle Fracture in Diabetics with Peripheral Neuropathy


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Connolly was the first to report on a series of patients with diabetes who developed limb-threateningdeformity or infection following failure of internal fixation of seemingly simple ankle fractures. Severalauthors have reported on high complication rates associated with ankle fracture in the population of patientswith diabetes, especially those with evidence of peripheral neuropathy. Several authors haveadvocated augmented internal fixation combined with prolonged non-weight-bearing until radiographicevidence of bony healing, based on case-controlled series. Many patients who present withCharcot arthropathy of the ankle initiated their disease process with an ankle fracture, often trivial andnon-displaced.

16.6.4 Charcot AnkleMost experts currently agree that when the destructive Charcot process involves the ankle joint, the resultantdeformity is so difficult to accommodate with orthotic means that amputation becomes inevitable whenstability/joint integrity is lost. Once the joint has been irreversibly damaged, early ankle or tibiocalcanealarthrodesis are advised. Biomechanical evidence suggests that internal fixation with a retrograde lockedintramedullary nail affords the most stable mechanical construct. While various applications ofblade-plating have been used to achieve ankle fusion in this complex patient population, it appears thatankle fusion with retrograde intramedullary nailing is currently the most popular technique to achieve anklearthrodesis. This technique is complicated by both early and late intramedullary infection thatrequires creative methods for successful resolution.

Stress fracture of the distal tibial metaphysis is a known complication following successful ankle fusion,regardless of the method of fixation. This can be avoided by extending the ankle fusion nail to theproximal tibial metaphysis.

16.7 ConclusionsCharcot foot is becoming a larger clinical problem due to the increased incidence of diabetes and morbidobesity and the improved longevity of affected patients. As the problem has become more apparent, theinterest of the orthopaedic device industry has provided improved implants for the surgical treatment of thisdisorder. Increasing incidence and awareness, combined with increased interest by orthopaedic foot andankle surgeons and improved implants appears to predict a more favorable future for this very complexpatient population.

16.8 Other Images


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Figure 2a.

Figure 2b.

Figure 2c.


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This 58-year-old patient, the owner of a construction firm, presented with a 2-week history of aFigures 2a-c.painful, swollen foot. He is clinically plantigrade, ie, he is weight-bearing on the normal plantar skin of thefoot.

Figure 2d.

Figure 2e.

Weight-bearing radiographs on presentation. The patient is radiographically plantigrade, ie,Figures 2d-e.the axis of the hindfoot (axis of talus as measured from weight-bearing AP radiograph) is reasonablycollinear with the axis of the forefoot (axis of the first metatarsal as measured from weight-bearing APradiograph). He was treated with a weight-bearing total contact cast, changed every 2 weeks until the footwas clinically stable and the swelling had resolved. The patient was then transitioned to therapeuticfootwear.


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Figure 2f.

Figure 2g.

Weight-bearing radiographs at 1 year. The patient has remained ulcer-free at 3 years.Figures 2f-g.

Figure 3a.


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Figure 3b.

Figure 3c.

This 77-year-old female had been treated in a series of non-weight-bearing casts for 9 monthsFigures 3a-c.prior to presentation. Note that she developed the ulcer from weight-bearing on the head of the talus.

Figure 3d.


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Figure 3e.

Figure 3f.

Non-weight-bearing radiographs at presentation.Figures 3d-f.


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Figure 3g.

Figure 3h.

||Figure 3i.


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1. 2.

3. 4.

5.

Photographs at 1 year. The patient wears standard therapeutic footwear and customFigures 3g-i.accomodative foot orthoses.

Figure 3j.

||Figure 3k.

The same patient's radiographs at 1 year.Figures 3j-k.

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Charcot Foot

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