Charcot Joint

Brandi Kimble D.P.M.

Basic Information

Definition

In 1708, William Musgrave first coined the term Charcot to describe arthralgia associated with neuropathic joints caused by venereal disease. In 1868, Jean-Martin Charcot described Charcot with neuropathic disease caused by syphilis. Charcot arthropathy is a progressive condition; the hallmark features include pathologic fractures, dislocations, and gross foot and ankle deformities that can lead to ulceration, infection, and possible amputation. Charcot arthropathy is commonly associated with diabetes and diabetic peripheral neuropathy. Early recognition and diagnosis are imperative to avoid severe and irreversible foot deformities that may lead to ulceration, amputation, and ultimately the demise of a patient.

Synonyms

Neuropathic arthropathy
Charcot osteoarthropathy
Charcot neuropathic osteoarthropathy
Charcot arthropathy
Charcot foot
Charcot’s joint

ICD-10CM CODES
M14.671	Charcot’s joint, right ankle and foot
M14.672	Charcot’s joint, left ankle and foot

Epidemiology & Demographics

Prevalence

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The estimated prevalence of Charcot arthropathy is 8% to 16% in the general population.
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Charcot is underdiagnosed by approximately 25%.
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Charcot arthropathy is seen in ∼29% of diabetics with sensory neuropathy and loss of protective sensation.
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Bilateral presentation is seen in 10% to 35% of patients.
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The midfoot is involved 70% of the time, followed by the forefoot and rear foot, each accounting for 15%.
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Patients with type 1 diabetes mellitus have a higher predisposition to Charcot arthropathy than patients with type 2 diabetes mellitus.
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Observed in the fifth decade in diabetes mellitus type 1; observed in the sixth decade in diabetes mellitus type 2.
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Unknown sex predilection and ethnic distribution.

Physical Findings & Clinical Presentation

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Acute phase: Erythema, edema, and calor. There is at least a 2° C temperature difference between the involved limb and the contralateral foot. May present with mild pain or discomfort. Bounding pedal pulses. Typically no radiologic osseous abnormalities are seen during the early acute phase.
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The tarso-metatarsal joints are most commonly involved, followed by the forefoot and rear foot; a deformity in the foot may lead to unstable foot architecture.
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As Charcot arthropathy progresses in the untreated state, joint dislocation/subluxation occurs.
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During the coalescence phase, there is a reduction in warmth, edema, and calor. Coalescence of osseous fragments, ankylosis of joints, and new bone formation also take place during this phase.
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In the remodeling phase, a fixed deformity classically known as the “rocker bottom” foot occurs.
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Ulcerations may appear at any time during the acute and chronic stages of Charcot arthropathy.

Etiology

The most common cause of Charcot arthropathy is peripheral neuropathy associated with diabetes mellitus (Fig. E1). Less common conditions associated with Charcot arthropathy include syphilis, alcoholism, spina bifida, poliomyelitis, Charcot-Marie-Tooth disease, leprosy, familial amyloid neuropathy, CNS/PNS tumors, pernicious anemia, cerebral vascular accident, lead poisoning, rheumatoid arthritis, multiple sclerosis, and trauma. Currently, three theories contribute to the etiology involved in this disease:

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Neurotraumatic theory: Unperceived trauma or injury to an insensate foot. Osseous destruction is the result of unperceived sensory neuropathy with continued ambulation and repetitive stress. This repetitive microtrauma can lead to extensive bone destruction resulting in joint subluxation, dislocation, and pedal deformity.
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Neurovascular theory: Autonomic neuropathy, particularly sympathetic denervation, leads to arteriovenous shunting. This increase of blood flow into the bone causes demineralization of the bone and stimulates osteoclastic activity that causes bone destruction, leading to osteopenia.
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Inflammatory theory: During the acute inflammation phase that is seen in Charcot arthropathy, the inflammatory cytokines, tumor necrosis factor-alpha, IL-1, and IL-6 are present. The role of these inflammatory cytokines is bone resorption by promoting osteoclastic proliferation and differentiation. Receptor activator of nuclear factor-kappa B ligand (RANKL) is responsible for activating osteoclasts in Charcot arthropathy. Osteoprotegerin is the antagonist of RANKL, and thus when this pathway is disrupted, osteoclastic activity predominates. The production of calcitonin gene-related peptide, which also antagonizes RANKL expression, is reduced in peripheral and autonomic neuropathy. Nitric oxide, which suppresses osteoclastic activity, has also been found to be dramatically decreased in Charcot arthropathy. Furthermore, advanced glycation end products are associated with increased RANKL activation. Hyperglycemia is the triggering factor for production of advanced glycation end products.

FIG.E1

Diabetes mellitus and neuropathic arthritis.

Note lateral displacement of metatarsals

Diagnosis

Differential Diagnosis

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Abscess
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Osteomyelitis
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Cellulitis
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Gout
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Deep vein thrombosis
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Infectious arthritis/septic joint
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Osteoarthritis
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Complex regional pain syndrome
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Peripheral vascular disease
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Trauma

Workup

A thorough history and physical examination is the key to recognition of Charcot arthropathy. Early diagnosis requires an astute physician to be aware of the signs associated with acute Charcot, including but not limited to edema, erythema, and calor, which play a role in the inflammatory cascade. Testing for peripheral neuropathy should be performed utilizing methods such as electromyography, nerve conduction velocity tests, nerve biopsy if warranted, biothesiometer, and Semmes-Weinstein monofilament testing.

Laboratory Tests

Laboratory testing can be utilized to rule in or rule out diagnoses that may present with manifestations similar to those of Charcot arthropathy.

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The following labs may be ordered if warranted: complete blood count with differential, basic metabolic panel, vitamin B₁₂, folate, RPR, ESR, CRP, uric acid, rheumatoid panel, joint aspiration, and bone biopsy.

Imaging Studies

Plain x-rays

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Plain x-rays may or may not show evidence of early osteomyelitis. Osseous findings will depend on the stage (inflammatory, development, coalescence, remodeling) of presentation of Charcot arthropathy.
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MRI can detect subtle changes in the early stages of active Charcot arthropathy.
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Three-phase bone scan: Results are less accurate in the setting of diminished blood flow; thus, labeled white blood cell scanning can improve specificity.
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Positron emission tomography is currently being researched for an additional imaging modality to detect Charcot arthropathy.

Treatment

Acute General Rx

The most instrumental aspect of medical treatment of Charcot arthropathy is offloading. Offloading is accomplished with the use of total contact cast for approximately 12 to 18 weeks pending clinical and radiographic assessment.

Once the acute phase has transpired, custom-molded Plastazote insoles in accommodative diabetic shoe gear, Charcot restraint orthotic walker, and customized braces, just to name a few, can be utilized.

Surgery

There is equivocal evidence to support whether surgical intervention is recommended during the acute phase of Charcot arthropathy. The general consensus for podiatric surgical intervention is for when there is acute fracture dislocation or infection, or when there is continued recurrence of ulceration. Arthrodesis is recommended for unstable pedal construct, and Achilles tendon lengthening to reduce forefoot pressure improves the overall pedal alignment.

Pharmacologic Therapy

Studies are currently being conducted to determine the efficacy of bisphosphonates whose mechanism of action is to decrease osteoclastic resorption and symptoms in active Charcot arthropathy.

Disposition

Early recognition of Charcot arthropathy is essential in preventing the devastating complications associated with this disease.

Referral

Podiatrist with expertise in Charcot arthropathy
Endocrinology for diabetic blood glucose control

Ferri – Charcot Joint