Vincent James Sammarco and G. James Sammarco
DEFINITION
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 will demonstrate 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 al14 (FIGS 1 AND 2).
FIG 1 • Classification of Charcot midfoot fracture-dislocation as described by Sammarco and Conti.
PATHOGENESIS
Peripheral neuropathy is most commonly related to diabetes but may occur with other neurologic disorders as well.
Glycosylation and diminished blood supply to the peripheral nerves result in progressive loss of sensation, motor innervation, and autonomic function.
Longer nerves are more severely affected, resulting in the typical “stocking and glove” sensory deficit.
Loss of protective sensation in the lower limb predisposes patients to ulceration and may make them oblivious to 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.
Intrinsic imbalance in the foot musculature also results in clawing of the hallux and lesser digits.
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 may be unaware or
FIG 2 • Classification of Charcot midfoot fracture-dislocation by Schon and Weinfeld.
unconcerned 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 a dorsal dislocation of the metatarsals. 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 Eichenholz.6
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.
In Stage III, bony consolidation 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. Commonly these increased soft tissue pressures, combined with the previously mentioned loss of protective sensation and loss of normal integumentary function, may lead to ulceration and potentially deep infection. In diabetics, these problems are 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.1–5,8–13 Standard arthrodesis techniques often fail in these patients due to the poor bone quality and significant fragmentation that accompanies these cases.15 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 Eichenholz 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 for these patients: 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 receiving dialysis have a much 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, who may not be able to mount an adequate immune response, and patients are often started on antibiotics at presentation. At the time of consultation, the patient has often already been admitted to the hospital with the initiation of intravenous antibiotics, bed rest with elevation of the extremity, and a non–weight-bearing status, thus blurring the ability to distinguish whether the patient improved due to simple rest or medications.
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 with a 5.07 SemmesWeinstein monofilament, 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.16 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 as 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).
FIG 3 • A 54-year-old man with Charcot midfoot fracture-dislocation. A. Clinical deformity. B. Lateral radiograph showing midfoot fracture-dislocation. C. Plantar ulceration recalcitrant to extended contact casting. (Reprinted with permission. Copyright 2006 Cincinnati SportsMedicine Orthopaedic Center.)
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. Radiographs alone are sufficient for diagnosing the disease process, but other imaging studies are often necessary to determine the presence or absence of infection.
MRI
MRI is frequently used to help determine the presence of osteomyelitis, but caution must be given to interpretation as the false-positive rate is very 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 above MRI findings should be considered diagnostic for deep infection.
CT
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 99m Tc 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.7
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 diagnosis of the underlying reason for 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
The majority of patients who develop noninfected Charcot arthropathy can be treated nonoperatively.
Nonsurgical treatment typically entails a period of cast immobilization using a total-contact cast, and possibly a period of limited or 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 Eichenholz stage III, the patient is fitted for accommodative orthotics and shoe wear. Accommodative devices may be as simple as an offthe-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
This technique involves passing large-bore cannulated screws across the uninvolved metatarsal heads through the metatarsophalangeal (MTP) joints and is contraindicated in patients without significant sensory neuropathy.
This technique is most useful for deformity at the tarsometatarsal level, and can be extended across the naviculocuneiform joints.
FIG 4 • Case example for technique demonstration: a 71-yearold woman with idiopathic neuropathy. A, B, C. Clinical photographs show midfoot deformity after spontaneous midfoot fracture-dislocation. Ulceration was present medially, which resolved after 6 weeks of contact casting. D, E. Preoperative clinical radiographs show dislocation at the tarsometatarsal joint. Gross instability was present on physical examination. (A, from Sammarco VJ, Sammarco GJ, Walker EW Jr, Guiao RP. Midtarsal arthrodesis in the treatment of Charcot midfoot arthropathy: surgical technique. J Bone Joint Surg Am 2010;92(Supplement 1 Part 1):1–19; printed with permission.)
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).
Positioning
The patient is positioned supine with a bump under the hip so that the toes face perpendicular to the operating table.
A pneumatic tourniquet is used at the thigh.
The patient is prepared and draped above the knee. A threestep tendo-Achilles lengthening, gastroc–soleus recession, or both is performed to achieve ankle dorsiflexion of 15 degrees before inflating the tourniquet.
Approach
A twoor three-incision approach is used to reduce deformity and to prepare the arthrodesis bed. A medial approach is used to expose the medial column.
The insertions of the tibialis anterior and posterior should be left undisturbed when possible, but they are often attached to fragmented or dislocated bone and should be secured with nonabsorbable suture placed in a locking fashion during the approach, for reattachment at closure.
A subperiosteal dissection is carried out above and below the level of the deformity. The middle column of the foot is approached though a dorsal incision centered between the second and third metatarsal bases.
Care should be taken to preserve the dorsalis pedis artery at this level. A third incision is usually necessary for exposure and reduction of the lateral column and is carried out dorsally at the level of the fourth and fifth tarsometatarsal joints.
Care must be taken to provide an adequate skin bridge between the dorsal incisions or wound necrosis or dorsal slough may occur.
TECHNIQUES
AXIAL SCREW TECHNIQUE FOR MIDFOOT ARTHRODESIS IN CHARCOT FOOT DEFORMITIES
Resection
Perform bone resection with an oscillating saw at the level of deformity.
Adequate bone resection is necessary to prevent excessive tension on the dorsal soft tissue envelope and vascular structures.
Bone resection is at the level of the deformity and usually involves resection of some bone from the proximal and distal fragments. Carry out bone resection medially for the medial column, and dorsally for the middle and lateral columns.
Remove bone from the dorsal incisions with a curved curette or pituitary rongeur. Adequate bone resection is indicated by the ability to manually reduce the deformity.
Resect bone slowly so that a balanced reduction can be achieved between the metatarsal bases. It is possible to resect so much bone that adequate bony apposition cannot be achieved for successful arthrodesis (TECH FIG 1A–C).
Place guidewires in the metatarsal shafts without crossing the apex of the deformity. This can be done retrograde through the MTP joints under fluoroscopic control, although this can be quite time-consuming and technically demanding. To pass retrograde guidewires, hold the MTP joint in hyperdorsiflexion and pass the wire under fluoroscopic guidance across the joint and into the metatarsal head and into the shaft. Alternatively, pass the guidewires antegrade though the apex of the deformity. After bony resection, flex the foot through the middle and enter the metatarsal base with a curved curette, then a guidewire, which is passed into the metatarsal shaft. Then dorsiflex the MTP joint and drive the wire out through the plantar skin distally. The fifth metatarsal can usually not be fixed axially because the intramedullary canal typically aligns lateral to the cuboid (TECH FIG 1D–G).
Ream the metatarsal shafts with cannulated drills. It is best to start with a small guidewire and a small cannulated drill and then change to a larger guidewire and larger cannulated drills. The medial column is usually drilled to 5.5 mm and a screw 6.5 mm or 8.0 mm in diameter is applied. The lesser metatarsals are usually drilled to 4.5 mm and a screw 4.5 mm or 5.0 mm is applied.
Once the guidewires are in place in the reamed metatarsal shafts, hold the deformity reduced and advance the guidewires into the midfoot. Measure screw length from the middle part of the first metatarsal head in the medial column, and from the metaphyseal–diaphyseal junction of the lesser metatarsals. A counter-sink must be applied through the metatarsal head or it may fracture as the screw head is applied. Use screws with reduced-diameter heads (TECH FIG 1H,I).
After applying the screws, sequentially tighten them to provide compression across the arthrodesis site.
Perform a layered closure. Close the skin with 3-0 nylon suture applied with vertical mattress technique. A drain is usually not necessary.
TECH FIG 1 • EUR Bone resection and exposure. A–C. Medial column is exposed: note the tibialis anterior tendon insertion, which must be reattached if it is released for reduction. The saw is used to resect bone plantarly and medially to restore axial alignment and to relieve soft tissue tension. D–G. Preparation of the intramedullary canals is done after the bone resection. Fluoroscopic control is used during wire placement and reaming. D, E.Medial column. (D, E, from Sammarco VJ, Sammarco GJ, Walker EW Jr, Guiao RP. Midtarsal arthrodesis in the treatment of Charcot midfoot arthropathy: surgical technique. J Bone Joint Surg Am 2010;92(Supplement 1 Part 1):1–19; reprinted with permission.) F, G. Middle and lateral columns. H. Application of the screws axially across the arthrodesis site after advancing the guidewires to the desired level. I. Intraoperative photograph of correction. J, K. Postoperative radiographs showing midfoot fusion without recurrence. L. Clinical photograph taken 1 year postoperatively. (G, H, J–L, from Sammarco VJ, Sammarco GJ, Walker EW Jr, Guiao RP. Midtarsal arthrodesis in the treatment of Charcot midfoot arthropathy: surgical technique. J Bone Joint Surg Am 2010;92(Supplement 1 Part 1):1–19; reprinted with permission.)
PEARLS AND PITFALLS
Treatment of midfoot arthropathy is controversial and most cases can be managed nonoperatively by casting and bracing.
Surgery is indicated for grossly instability, recurrent ulceration, a nonplantigrade foot and unbraceable deformity.
When surgery is done: span the area of dissolution; adequate bone resection, use bigger, stronger implants; place implants where they offer mechanical advantage.
Keys to success: do not operate on dysvascular limbs, eradicate infection/ulcer prior to applying internal fixation, aggressive surgical treatment of equinus, get a good correction.
POSTOPERATIVE CARE
The patient is placed in a well-padded posterior splint postoperatively. This is typically changed within a few days of the surgery and switched to a cast.
The patient is non–weight-bearing for 10 to 16 weeks, and may begin weight bearing in a pneumatic walking boot once bony consolidation is evident radiographically (average 12 weeks).
Once edema and swelling are under control, the patient may be graduated to diabetic shoe wear with a custom multidensity foam orthotic.
Techniques Figure 1J–L shows postoperative radiographs and a photograph.
OUTCOMES
The authors reported on 20 patients followed for an average of 49 months (range 20 to 77 months).17
Complete arthrodesis of all joints was noted in 75% of patients and partial fusion with stable correction was noted in all patients.
There were five hardware failures and three patients required removal of screws that backed out partially.
All patients returned to functional status with diabetic shoe wear and orthotics. None required above-ankle bracing.
There were no amputations.
COMPLICATIONS
Screw loosening, backing-out, and hardware failure may occur as fixation will sometimes cross uninvolved joints. The surgeon should avoid crossing the calcaneocuboid and talonavicular joints when possible. Crossing uninvolved joints is acceptable when necessary to achieve adequate fixation in neuropathic patients. Radiographs should be monitored carefully when weight bearing is initiated as screws will sometimes bend before failing and can be exchanged percutaneously. Screws that back out into the ankle or MTP joint should be removed or exchanged.
Overcorrection can occur and may result in ulceration beneath the first metatarsal head.
Partial nonunion may occur and does not need to be treated as long as the foot is plantigrade. All patients in our series maintained the majority of their correction at final follow-up.
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