Surgical Stabilization of Nonplantigrade Charcot Arthropathy of the Midfoot

Charcot foot arthropathy is an inflammatory disease process that primarily affects the foot and ankle of patients with long-standing diabetes (10-plus years) and diabetic peripheral neuropathy (PN).^3,4,7,24

The destructive inflammatory process often leads to bone destruction and joint subluxation or dislocation. The hallmark clinical deformity is known as a rocker bottom deformity.

The resulting disabling deformity impairs walking, can be painful, and makes patients prone to develop overlying pressure-induced wounds which lead to deep infection and the eventual need for lower extremity amputation.²⁶

Treatment has historically involved immobilization in a total contact non–weight-bearing cast during the acute destructive phase, followed by longitudinal management with accommodative shoes, foot orthoses, and ankle–foot orthoses.¹³

Even when this treatment is successful, the negative impact on health-related quality of life has been demonstrated to be similar to lower extremity amputation.^6,17

This observation has led most experts to currently recommend surgical correction of the acquired deformity to avoid skin breakdown and deep infection, allow use of commercially available therapeutic footwear, avoid amputation, and maintain walking independence.^15,24,25

This chapter will present an evidence-based algorithm for use in the management of Charcot foot arthropathy at the level of the midfoot.

ANATOMY

The foot is a unique terminal end organ adapted for weight bearing.

The multiple linked small bones of the normal foot allow prepositioning of the durable plantar soft tissue envelope to accept the loading forces associated with weight acceptance and then become a stable launching platform for push-off.

The bone and joint destructive associated with Charcot foot arthropathy impairs the capacity to orient the foot in the optimal position to perform these tasks.

The ensuing deformity induces weight bearing through less durable tissues, leading to soft tissue failure, ulceration overlying bony prominences, destructive osteomyelitis, and ending with systemic sepsis or need for lower extremity amputation.

PATHOGENESIS

The key clinical risk factor associated with the development of Charcot foot arthropathy is long-standing diabetic peripheral neuropathy as measured by insensitivity to 10 g of applied pressure with the Semmes-Weinstein 5.07 monofilament (FIG 1).

Peripheral neuropathy associated with alcohol abuse has been suggested as an initiator of the destructive disease process; however, many of these patients are eventually confirmed to be diabetic. Patients with peripheral neuropathy secondary to chemotherapy or other drugs are unlikely to develop Charcot foot arthropathy.

The true pathophysiology of Charcot foot arthropathy is likely a combination of both neurotraumatic and neurovascular theories. The inciting trauma can be a single event, that is, fracture or dislocation or repetitive microtrauma combined with the neuropathy-induced motor imbalance that creates an equinus moment at the midfoot level. Arteriovenous (AV) shunting in the bone of patients that have been demonstrated to be vitamin D deficient and osteoporotic leads to mechanical failure. Loss of protective sensation allows morbidly obese patients to continually load the mechanically weak bone, which fails, depending on the direction of the applied force vectors, leading to a clinical scenario that mimics hypertrophic nonunion or malunion.

Trauma appears to be the trigger that initiates the destructive inflammatory process.²⁴ The high association of morbid obesity in symptomatic patients would suggest a mechanical component.¹⁸

Although the presence of sensory PN is well recognized, the accompanying motor and vasomotor neuropathies are often overlooked. The motor neuropathy affects the smaller nerves and muscles of the anterior leg (foot and ankle dorsiflexors) earlier in the disease process than the posterior leg compartments, leading to a motor imbalance and an equinus-induced bending moment at the level of the midfoot. The autonomic neuropathy leads to increased swelling, making the tissues less resistant to the applied shearing forces during walking.

Baumhauer et al¹ has demonstrated, via histochemical studies, the cytokines involved with the initiation of the destructive inflammatory process.²⁴

NATURAL HISTORY

It is currently estimated that Charcot foot arthropathy occurs at a rate of approximately 0.3% per year in the overall diabetic population.⁸ Many patients are misdiagnosed with gout, tenosynovitis, cellulitis, or deep infection.²⁰ The symptoms will spontaneously resolve in many of these patients, making determination of the true incidence difficult.⁸ It is likely that those patients who are morbidly obese are more likely to become symptomatic.

Eichenholtz⁷ in 1966 published a detailed monograph based on his observations in 66 patients over a 30-plus year career. This clinical, radiographic, and histologic observational monograph provides valuable benchmark information on the development and progression of this destructive disease process.⁷

Longitudinal data would suggest that the health-related quality-of-life impact of Charcot foot arthropathy is similar to that of a transtibial amputation.^6,17,23

PATIENT HISTORY AND PHYSICAL FINDINGS

The classic presentation is a grossly swollen, painless foot, without a history of trauma, in a mid-50s to mid-60s morbidly obese long-standing diabetic. Many patients remember a specific traumatic event, although it might be trivial (FIG 2).^14,18,21 It is common for Charcot foot arthropathy to develop following fracture or dislocation.

The key element appears to be the presence of peripheral neuropathy as measured by insensitivity to the Semmes-Weinstein 5.07 (10 g) monofilament (see FIG 1).

Classically described as painless, many patient have pain associated with the onset.

Many describe a feeling of clicking or “crunching” at the involved site, associated with the development of instability. Palpable painless joint instability is present at this time.

The foot is typically swollen, erythematous, and warm.

IMAGING AND OTHER DIAGNOSTIC STUDIES

Treatment can be determined based on clinical examination and plain weight-bearing radiographs.

Eichenholtz⁷ arbitrarily categorized the timeline of the disease process into three stages.

Stage I is the early active stage of the disease process. The foot is swollen, warm, and erythematous. Radiographs are normal.

Stage II is entered when there is sufficient destruction of the ligamentous structures of the involved joints or bony weakness to allow joint dislocation and/or periarticular fracture. A healing response will often develop during this destructive phase of the disease process, prompting other authors to divide the disease process into more stages. This is when the radiographs take on the characteristic appearance of hypertrophic destruction with or without bony repair. One can conceptualize this stage somewhat similar to that of a hypertrophic nonunion.

Stage III is the consolidation of the destructive process. The resultant deformity will develop based on the mechanical loading during the active phase. Radiographs will assume a classic posture of deformity and/or hypertrophic nonunion.⁷

Nuclear scanning is rarely helpful in distinguishing acute Charcot foot arthropathy from diabetic foot infection or abscess.

Magnetic resonance imaging is occasionally beneficial when it demonstrates bony destruction contiguous to a wound.

DIFFERENTIAL DIAGNOSIS

In the least destructive presentations of the disease process, patients are frequently misdiagnosed with a deep venous thrombosis, cellulitis, acute gout, or tenosynovitis.²⁰

Although patients have evidence of peripheral arterial disease, as evidenced by calcified pedal or leg arteries, pedal pulses are generally bounding and ultrasound Doppler studies are normal.

The critical differential is foot abscess.

Patients with Charcot foot arthropathy do not respond to antibiotic therapy. Patients with a diabetic foot abscess, or infective cellulitis, will admit to malaise as opposed to those with Charcot foot arthropathy who do not demonstrate constitutional symptoms.

The first sign of occult infection in the diabetic is increasing blood sugar or increasing insulin demand. White blood cell count may not increase, as these patients are often poor hosts and are not capable of mounting a normal immune response.

Patients with deep infection will generally have an entry portal for infection, which might be as simple as an infected ingrown toe nail or a crack or pinhole between the toes.

Patients with acute Charcot foot arthropathy will have normal blood sugar levels (for the individual patient) and will not have open wounds or purulent drainage.

The erythema that is present in the diabetic patient with acute Charcot arthropathy will disappear with elevation, in contrast to the patient with an abscess or deep infection.

NONOPERATIVE MANAGEMENT

Classically, treatment has been accommodative with a non–weight-bearing total contact cast during the acute phase. Long-term management has been accomplished with accommodative bracing. Surgery was only advised for bony infection or when orthotic management could not accommodate the acquired deformity.

Patients who are clinically and radiographically plantigrade can be treated with a weight-bearing total contact cast during the active phase of the disease process.^5,21 The cast should be changed every 2 weeks until the volume of the limb stabilizes and the foot is sufficiently stable to transition to therapeutic footwear (FIG 3).^5,21