Charcot Neuroarthropathy

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Charcot neuroarthropathy is a noninfectious progression of joint destruction characterized by pathological fractures and joint dislocations. Although it was initially described by Musgrave in 1704, its name was attributed to J.M. Charcot in 1868 (116). The disease involves joint destruction of accompanying common diseases that manifest with peripheral neuropathy, such as leprosy, tertiary syphilis, chronic alcoholism, and spina bifida (117). Diabetes mellitus is currently the primary cause of Charcot neuroarthropathy.


The exact etiology of Charcot neuroarthropathy remains unclear. There are two leading theories: the neurotraumatic (German) theory, and the neurovascular (French) theory. The neurotraumatic theory proposed that repeated microtrauma on neuropathic joints results in the eventual joint destruction (118). Repetitive minor stresses on insensate joints produce intracapsular effusions, ligamentous laxity, and joint instability. With continued use of the foot, degeneration of the joints continues, often resulting in severe joint dislocation, fractures, and deformity mostly because of arch collapse.

In contrast, the neurovascular theory suggested that the main factor is the autonomic neuropathy-related hyperemia that causes excessive bone resorption and leads to weakening of the bone (119). The hyperemic bone resorption thus allows for increased risk of fractures with joint dislocation and destruction evident in Charcot joints. This theory corresponds to the clinical observation that Charcot neuroarthropathy occurs most commonly in patients with palpable pedal pulses (120). Further support to this hypothesis is provided by studies in the unit that have shown that the nonspecific hyperemic response to skin heating is increased in patients with neuroarthropathy, when compared with patient with diabetes with equally severe neuropathy (54). The current consensus is that the process of Charcot neuroarthropathy is secondary to a combination of both the neu-rovascular and neurotraumatic theories.

Clinical Findings

Regardless of the exact etiology, the Charcot foot usually presents as a warm, non-painful, swelling of the foot. Usually, there is no evidence of an open wound and an infectious process, although often suspected it can be excluded based on lack of clinical findings to support infection. Occasionally, patients may describe a precedent history of minor trauma; however, this is frequently so trivial that the patient is unable to recall the incident. Trauma in the form of foot surgery can also be another precipitating factor. The Charcot neuroarthropathy can occur in either the ipsilateral or contralateral limb following foot surgery. This phenomenon can be attributed to the likely alteration in weight-bearing forces in joints of the foot, triggering the changes in Charcot joint.

Initial evaluation of Charcot neuroarthropathy requires a thorough clinical and radi-ographical examination of the foot. Clinical examination reveals a warm, edematous foot often with evidence of crepitus with joint range of motion of the affected joint. Joint laxity is often present. Most commonly, pain is absent or significantly less than expected from the clinical presentation. Radiographical findings may reveal a spectrum of findings from subtle subluxation to frank dislocation with osseous debris and fragmentation. The most common site affected in the foot is the tarsometatarsal joint (121). The extent of fragmentation and joint destruction is variable and most often related to the particular joints affected and the degree of ambulation before the diagnosis. Advanced imaging techniques, such as CT scans and magnetic resonance imaging are rarely necessary to make the diagnosis of Charcot joint especially in advanced cases and instead may be more useful in preoperative surgical planning in certain cases.

There are three identifiable clinical phases of Charcot neuroarthropathy: acute, coalescence, and remodeling. The acute phase is characterized by clinical findings of edema, erythema, localized warmth, and joint crepitus with range of motion examination. The coalescence phase begins when skin temperature normalizes and joint crepi-tus diminishes. With a period of duration lasting from months to years, the remodeling phase is characterized by joint stabilization and remodeling.

Resolution of Charcot neuroarthropathy can result in a deformed foot with obvious bony prominences susceptible to ulceration (Fig. 9) (122). If diagnosed early and sufficient immobilization is rendered, the possibility of joint collapse with resulting osseous prominences may be mitigated. However, in instances of misdiagnosis or inadequate immobilization, a "rocker-bottom" type foot can result, with gross deformities of the involved joint and prominent areas to the plantar aspect of the foot. These prominent areas often on the plantar aspect of the midfoot are prone to increased pressure and ulceration.


The treatment of choice for acute Charcot foot is complete immobilization and non-weight-bearing. Immobilization can be achieved with casts, splints or braces, and non-weight-bearing aid with the use of crutches, walkers, or wheelchairs. Failure to adequately immobilize the foot might result in furthermore fragmentation of bone with progression of

Charcot Foot
Fig. 9. (Continued)

the joint deformity, resulting in a nonplantigrade foot. The ultimate goal of immobilization therapy is to allow for the foot to coalesce in a shape that will allow for eventual ambulation.

Immobilization and nonweight-bearing should continue until the acute phase of Charcot has ended and the coalescence phase commenced. The duration of immobilization varies from 8 to 32 weeks (123,124). The decision to begin weight-bearing may be best made by clinical parameters such as foot temperature (should be the same with the contralateral limb) and resolution of erythema and edema, rather than an arbitrary time period. Serial radiographs may also aid in the decision making process. Evidence

Common Feet Deformities

Fig. 9. (A) Midfoot Charcot neuroarthropathy in a patient with diabetes with severe peripheral neuropathy. Severe foot deformity has resulted to an area where high pressures have been applied during walking leading to extensive ulceration. (B) X-ray from the same patient shows extensive destruction of the midfoot joints.

Fig. 9. (A) Midfoot Charcot neuroarthropathy in a patient with diabetes with severe peripheral neuropathy. Severe foot deformity has resulted to an area where high pressures have been applied during walking leading to extensive ulceration. (B) X-ray from the same patient shows extensive destruction of the midfoot joints.

of osseous consolidation, union of fractures, and reduction in soft tissue edema are radi-ographical clues that coalescence has begun.

Once weight-bearing is deemed safe, return to ambulation should be performed in a gradual manner. Typically, weight-bearing is begun allowing only 15-20 pounds of weight on the affected limb, with 10 pound increments added on a weekly basis. Should symptoms of the acute phase, such as edema, erythema, and warmth appear, immobilization and nonweight-bearing should be resumed until resolution of these symptoms occur. As weight-bearing progresses, the patient is eventually allowed to fully ambulate short distances without the use of assistive devices.

In recent years, increased attention has been given to surgical reconstruction of the severely deformed Charcot foot. In cases where immobilization and nonweight-bearing have failed to prevent extensive joint dislocation, a rocker-bottom type foot with osseous prominences can be the end result. This type of foot is highly susceptible to ulceration. Therefore, arthrodesis of the involved joints might provide a stable platform for ambulation in addition to preventing future ulcerations. However, patients undergoing joint fusions will require extended periods of postoperative immobilization and nonweight-bearing, and therefore, should be screened carefully. Arthrodesis in patients who are identified early before advanced bone destruction occurs is gaining especially in compliant patients (125).

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  • mya
    What reverses charcot foot?
    7 years ago

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