Axial Screw Technique for Midfoot Arthrodesis in Charcot Foot Deformities

Fracture through the midfoot in the neuropathic patient may accompany minor or incidental trauma and if unchecked may lead to severe deformity or “rocker bottom” foot deformity.

This chapter demonstrates a technique used for fusion of the unstable midfoot fracture-dislocation.

ANATOMY

Charcot fracture-dislocation of the midfoot may occur through the tarsometatarsal, intercuneiform, or transverse tarsal joints.

Multiple patterns may exist and are often complicated by bony dissolution. Attempts to classify these dislocations have been described by Sammarco and Conti¹¹ and Schon et al¹⁵ (FIGS 1 and 2).

PATHOGENESIS

Peripheral neuropathy is commonly related to diabetes but may occur with other neurologic disorders as well.

In diabetic patients, glycosylation and diminished blood supply to the peripheral nerves result in progressive loss of sensation, motor innervation, and autonomic function.

Loss of protective sensation in the lower limb predisposes patients to ulceration and may make them unaware of fractures or dislocations.

Loss of motor function leads to intrinsic imbalance of muscles in the lower extremity and commonly leads to equinus contracture of the ankle and Achilles, which significantly increases the forces through the foot during gait.

Autonomic sensory loss results in drying and cracking of the skin, which diminishes integumentary protection from pathogens.

Autonomic dysfunction also is responsible for loss of vasomotor control, which may lead to edema and stasis.

NATURAL HISTORY

Midfoot fracture-dislocation in the insensate patient may result acutely from direct trauma but more commonly is due to repetitive microtrauma in insensate joints. Once instability develops, bony deformity usually follows and worsens due to neurally stimulated vasomotor response, which increases blood flow to the area and leads to bony dissolution. Because the process is typically painless, the patient is often unaware that a problem is present until massive soft tissue swelling, gross deformity, ulceration, and infection are present.

Fracture and dissociation through the midfoot may progress to dislocation of the metatarsals and tarsal bones. Once bony dissociation occurs, contracture of the soft tissue envelope makes reduction of the deformity difficult or impossible without surgical resection of bone at the fracture site.

Charcot neuroarthropathy was staged by Eichenholtz.⁴

Stage I is the inflammatory stage. The foot is hyperemic, swollen, and hot. Bony dissolution and fragmentation may be present on radiographs.

Stage II is the coalescence phase, where swelling and edema decrease, temperature decreases, and redness improves.

Stage III is the osseous consolidation phase, where bone density begins resolving and fracture healing occurs, often with significant residual deformity.

Deformity at the level of the midfoot is poorly tolerated and leads to a significant increase in localized plantar pressures at the apex of the deformity. Increased localized pressures, combined with the previously mentioned loss of protective sensation and loss of normal integumentary function, may lead to ulceration and deep infection. In diabetics, these problems may be worsened by impaired circulation and immunologic function and can lead to amputation of the limb. If osteomyelitis develops, limb salvage may still be possible, but the risk of amputation is greatly increased.

This technique is one of a series of evolving techniques aimed at reconstructing these significant deformities.^{1–3,6–10,12,14} Standard arthrodesis techniques often fail in these patients due to the poor bone quality and significant fragmentation that accompanies these cases.¹⁶ The goals of this technique are to aid in reduction of deformity and to allow the fixation devices to bridge the area of dissolution at the apex of the deformity, achieving fixation in more normal bone proximally and distally.

PATIENT HISTORY AND PHYSICAL FINDINGS

The patient with Charcot neuroarthropathy of the foot may present in any of the Eichenholtz stages, but by far, the most common presentation to the orthopaedist is the inflammatory stage, with presumed cellulitis and osteomyelitis.

A history of trauma may or may not be present. Stage I and II patients will present with a swollen, red, and warm foot. Patients presenting to the orthopaedist in stage III will typically have a stable deformity that may or may not be amenable to bracing.

Prognosis is significantly affected by four things: the presence of infection, the presence of adequate blood flow in the extremity to the level of the digits, the presence of chronic venous stasis with associated poor integument, and the ability for the patient to adequately control his or her medical comorbidities. Patients who are immunocompromised due to transplant or those requiring renal dialysis have a worse prognosis than those with diabetes alone.

The presence or absence of infection must be established at the onset of treatment. This may be difficult as many of the physical signs of stage I Charcot deformity are indistinguishable from an infection.

Lack of constitutional symptoms does not preclude infection in diabetics. These patients may not be able to mount an adequate immune response. Clinical confusion can occur because at the time of consultation, the patient may have been admitted to the hospital with the initiation of intravenous antibiotics, bed rest with elevation of the extremity, and a non–weight-bearing status. This may blur the ability to distinguish whether the patient is improved due to simple rest and off-weighting or due to the antibiotics.

A history of fevers and chills, inability for diabetics to control their blood sugar levels, and a history of previous or current ulceration increase the likelihood of active infection at presentation.

The physical examination should document the presence or absence of pulses.

Neuropathy should be documented and the level of intact sensation should be noted in the patient’s record.

Protective sensation may be present even with Charcot neuroarthropathy. Any ulceration should be carefully documented as well as its depth and Wagner grade.¹⁷ The presence of fluctuance may be suspicious for abscess, and crepitation of the skin may represent gas gangrene; both require prompt diagnosis and surgical treatment. It is important to evaluate the contralateral foot and ankle as well or the patient may have pathology that is unrecognized.

Items in the history that suggest that surgical stabilization may be required include gross instability on physical examination, acute fracture-dislocation from trauma, and recurrent ulcerations despite appropriate nonoperative treatment (FIG 3).

IMAGING AND OTHER DIAGNOSTIC STUDIES

Radiographs

Radiographs of the ankle and foot should be taken (weight bearing when possible) to help stage the deformity.

Typical radiographic changes include fracture and dislocation, bony destruction, periosteal reaction, and malalignment.

These findings are difficult to distinguish from acute or chronic osteomyelitis and alone are unreliable for determining the presence or absence of infection.

Magnetic Resonance Imaging

A magnetic resonance imaging (MRI) is frequently used to help determine the presence of osteomyelitis, but caution must be given to interpretation as the false-positive rate is high. Bone destruction and bone and soft tissue edema may be present in Charcot neuroarthropathy without infection and alone should not be used to determine the presence of infection.

Enhancement with intravenous gadolinium gives stronger support to the presence of infection.

The presence of a fluid collection consistent with abscess formation or air associated with Charcot deformity and the earlier described MRI findings should be considered diagnostic for deep infection.

Computed Tomography

Computed tomography (CT) scan may show extensive bony destruction, periosteal reaction, and malalignment.

The use of CT is unnecessary for diagnosis, but it can be helpful in surgical planning.

The presence of air on a CT scan is considered diagnostic for deep infection and may represent with gas gangrene, or more commonly communication with an ulcer.

Nuclear Imaging

Nuclear imaging is particularly useful in helping differentiate an infected Charcot process from a noninfected process.

A three-phase technetium bone scan alone will be of little value as increased uptake will usually be present in all three phases. However, when this study is immediately followed by a labeled white blood cell scan, the combined studies can be useful to decide whether the process is Charcot process alone, soft tissue infection, or osteomyelitis.

Other isotopes may be useful in differentiating infection from a sterile Charcot process and include ^99mTc sulfur colloid and combined bone and white cell “dual peak imaging.” A detailed discussion of nuclear imaging is beyond the scope of this text, and the reader is referred elsewhere for further study.⁵

Electrodiagnostic Testing

This is usually unnecessary when peripheral neuropathy can be documented on physical examination.

Electrodiagnostic testing can be useful in patients who have relatively normal sensory examination but whose radiographic and clinical findings are suggestive of neuropathic arthropathy. It is useful for documentation of deficits and also may be helpful in determining the underlying diagnosis causing the neuropathy.

Vascular Testing

We recommend rigorous workup of any suspected vascular insufficiency. This usually entails screening with noninvasive arterial examination in patients who do not have readily palpable pulses on physical examination.

Arterial insufficiency is a relative contraindication to surgical reconstruction. Referral to a vascular surgeon should be considered for staged arterial reconstruction if significant insufficiency is present.

DIFFERENTIAL DIAGNOSIS

Osteomyelitis, acute or chronic

Abscess or gangrene

Traumatic dislocation

NONOPERATIVE MANAGEMENT

Most patients with noninfected Charcot arthropathy can be treated nonoperatively.

Nonsurgical treatment typically entails a period of cast immobilization using a total-contact cast and a period of non–weight bearing.

The goal of nonsurgical treatment with casting is to have the foot consolidate to a plantigrade structure without significant bony prominence.

Once the foot has entered Eichenholtz stage III, the patient is fitted for accommodative orthotics and shoe wear. Accommodative devices may be as simple as an off-the-shelf Plastazote orthotic if there is little residual deformity. More commonly, there is some deformity and the patient will require a custom-molded multidensity foam orthotic.

A Charcot restraint orthotic walker (CROW) is necessary if there is severe deformity.

Surgery is typically reserved for patients with acute fracture-dislocations, those with progressive or unbraceable deformities, and those with recurrent ulceration despite multiple attempts at accommodative bracing.

SURGICAL MANAGEMENT

Preoperative Planning

It is important to establish the absence of infection. Active infection or osteomyelitis is a contraindication for this technique as the hardware is typically permanent and difficult or impossible to remove without significant bony destruction. As noted previously, vascular workup is necessary before the procedure.

The involvement of an astute internist is important in control of diabetes and medical comorbidities. The timing of surgery is important. Acute trauma without bony dissolution or significant swelling can be safely reduced and fused within a week or two of injury, providing the dislocation is recognized and the patient has not entered the inflammatory stage of the neuroarthropathy process.

Once the patient enters the inflammatory phase, we prefer to cast the patient for 6 to 8 weeks to allow the edema to resolve and perform the reconstruction in a staged manner.

Indications

Treatment of unstable neuropathic foot dislocation

Treatment of patients with stable, nonplantigrade deformity who have recurrent ulceration at the apex of the deformity and who have not been responsive to custom bracing and shoe modifications

This technique involves passing large-bore cannulated screws across the uninvolved metatarsal heads through the metatarsophalangeal (MTP) joints and is contraindicated in patients with normal sensory function.

This technique is most useful for deformity at the tarsometatarsal level and can be extended across the naviculocuneiform joints.

A higher rate of failure, screw breakage, and nonunion is associated with fusions that cross the transverse tarsal joint, and extended non–weight bearing may be required to achieve fusion at this level (FIG 4).