When a reconstructed Charcot foot becomes unstable, physicians face a dilemma for salvaging the foot, given the complexity of the condition. Accordingly, these authors discuss key considerations and offer pertinent pearls for revisional and failed Charcot repair.
As the need for reconstruction of the Charcot foot increases across the population, surgeons are successfully and dramatically improving useless limbs via increasingly sophisticated techniques of foot and ankle surgery. The purpose of this article is not to describe primary Charcot repair but we will instead focus on the revisional and failed Charcot repair.
Before we discuss a treatment algorithm, it is essential to describe the distinction between a revisional procedure versus a failed Charcot reconstruction. We can define the failure of Charcot reconstruction as the inability to reconstruct a Charcot deformity adequately due to major overriding complications, including extensive osteomyelitis, hardware failure and a dysvascular foot.1 Charcot failure is a distinct entity from revisional Charcot reconstruction, which may encompass the same complications but to a lesser severity, enabling surgeons to undertake a revisional procedure.
The nature of Charcot arthropathy alters one’s definition of a successful outcome in Charcot reconstruction. A post-op pseudarthrosis is a failed surgical outcome in a healthy patient but that same pseudarthrosis may not be a failure in the Charcot patient as long as it is stable and non-edematous. A diagnosis of failure is therefore different for this population of patients just as a diagnosis of success is different.
For a successful outcome in diabetic Charcot reconstruction, the surgery typically requires the surgeon to achieve the following:
1. A foot with no open ulcers or any tendency to develop open ulcers during gait
2. A foot that fits into at least diabetic foot gear
3. A foot that permits the patient to be ambulatory
4. A foot that is not prone to collapse or recurrent instability
5. A foot that is least plantigrade and optimally has a medial longitudinal arch, and no bulging cuboid or medial cuneiform
6. A limb that can have its edema controlled with standard support hose or other simple means
7. A limb that is not painful or a burden to the patient
The management of a failed Charcot reconstruction parallels that of other revisional reconstructive foot and ankle surgeries. The most demonstrable difference is the extremely compromised state of these patients. These patients are significantly immunocompromised with advanced neuropathy and in many cases, they present with arterial insufficiency and some degree of renal insufficiency. It is obvious that this population has limited reserves for healing. Accordingly, it is incumbent upon the surgeon to evaluate all potential comorbidities prior to proceeding with further management of a revisional Charcot reconstruction.
Evaluation of the patient’s general medical status is absolutely essential to begin the workup for surgical re-intervention. Optimization of blood panels is paramount. We see many patients with HbgA1c far greater than 10%. Such poor control makes it very difficult for antibiotics or the patient’s own white blood cells for that matter to work in this population. The hospitalist or internist needs to take an active role in the management of these patients. Optimization of blood glucose, vitamin D, calcium, phosphate, control of hypertension and, in many instances, cardiac workup, are necessary.2
Although earlier literature postulated that patients with a Charcot diabetic foot by definition had satisfactory or even hyperemic circulation, clinical practice has proven this theory false in many cases.3 Patients with diabetic Charcot frequently have significant peripheral arterial disease (PAD).4 When a Charcot reconstruction fails due to wound dehiscence or infection, it is mandatory to reevaluate the vascular status as soon as possible, performing non-invasive studies including toe pressures and the ankle brachial index (ABI), and giving early consideration to angiogram and endovascular attention by vascular specialists.
It has been the senior author’s experience that patients who had intact circulation preoperatively and were cleared by vascular specialists can go on to have an occluded superficial femoral artery, tibial artery or other vessels during the perioperative period, producing resultant significant infection and/or wound dehiscence.
Serious postoperative infections compromise the outcome and cause failure in diabetic Charcot reconstructions. One must have a high level of suspicion for infection for this population of patients. These types of patients need very frequent follow-up throughout the perioperative period, more so than other patients. If the patient is home, there should be evaluation by home health nurses at least twice a week as well as a visit to the office. This may preclude a failure by early intervention.
A general rule that the senior author has used is that a postoperative diabetic foot infection is generally twice as bad as it looks on the surface. The surgeon needs to remember that neither an elevated white blood cell (WBC) count nor an elevated temperature is necessarily associated with a serious diabetic foot infection. Better measures of the severity of the infection include erythrocyte sedimentation rate (ESR) and the C-reactive protein (CRP). These are two tests that one must obtain and can use during therapy to identify progress or the lack thereof. As a rule, failure of Charcot reconstruction with infection requires prompt hospitalization. Infectious disease consultation is mandatory. Typically, imaging studies for Charcot include plain films and WBC labeled scans.
Implanted hardware, which one typically sees postoperatively in Charcot, negates magnetic resonance imaging (MRI) as a diagnostic tool to assess the severity of an infection. Furthermore, even if the patient had no hardware implanted whatsoever, MRI cannot discern between Charcot and infection.
Once one has diagnosed the infection clinically, the patient requires prompt surgery to remove all hardware, which is potentially infected. Obtain deep cultures during the surgery as well as a bone biopsy. All defects should receive pulse lavage. The surgeon needs to remove all avascular and dead bone. There are a variety of choices for wound management including VAC Therapy (KCI), wet-to-dry dressings or the use of antibiotic beads loaded with vancomycin or tobramycin. When possible, one can consider closure of the wound over the antibiotic beads with a drain. In some instances in which skin necrosis precludes primary closure, the physician may use a combination of antibiotic beads and VAC Therapy.
In these complex instances, placement of an external fixator is extremely beneficial. The frame provides access to the wounds, which a cast prevents. The fixator provides stability, which diminishes edema and the spread of infection, and it maintains normal architecture during healing.
Usually, these patients require at least six weeks of parenteral antibiotics in combination with local wound care. If complex wounds are present, the foot and ankle surgeon may elect to repair them during this period or refer patients to a plastic surgeon as indicated. One can exchange antibiotic beads every two weeks to deliver higher loads of antibiotic directly to the infected site. The decision to terminate antibiotic therapy and this convalescent part of the treatment should be based on the clinical appearance of the wound, perfusion of the wound, negative cultures and viability of the wound during debridement. The vascular status needs to be optimal before proceeding.
Subsequent to this, the surgeon can remove the external fixator and lay internal beams to recreate the transverse arches of the foot and the medial and lateral column. In the senior author’s practice, the beams do not attempt to create compression arthrodesis. Beams only facilitate alignment. The surgeons can place an external Ilizarov frame using bent wire technique to compress for fusion. Studies have documented that bent wire compression and internal screws provide synergistic compression superior to using screws alone.5,6
Closure should happen over drains. One should get input from an infectious disease physician as to the length of time to treat the wounds after hardware has been reintroduced.
Generally, patients require monthly laboratory studies including ESR and CRP for six months. Perform a WBC scan every six months or until the results are normal. Repeat X-rays are necessary to follow maturation of the surgical construct.
It has been the senior author’s experience that Charcot ankle reconstruction poses special challenges when a Charcot ankle surgery fails. In many instances, it is due to a hardware failure. Specifically, instances in which tibiocalcaneal nails have fractured through the ankle or calcaneus due to nonunion represent serious failure circumstances. This special class of failure requires removal of all hardware and placement of an Ilizarov external fixator frame with compression. It has been the senior author’s experience that it may be necessary to wait as long as 15 to 26 weeks for a solid fusion or a stable pseudarthrosis to evolve. When there is a failure of the primary ankle fusion in Charcot, the senior author’s preference is external fixation without further hardware introduction.
If after 20 to 26 weeks the ankle is still unstable, the senior author typically adds multiple large diameter stainless steel screws at different angles around the ankle to absorb the bending moments of the ankle. Most tibiocalcaneal nails rely on solid arthrodesis to work successfully over time.
One must take special precautions for patients with end-stage renal disease and abnormalities of bone metabolism associated with renal failure. A useful diagnostic test to determine if patients are capable of mineralizing bone is a serum osteocalcin level. A negative serum osteocalcin level predicts an inability in this population to heal bone and is a worrisome sign. The assistance of an endocrinologist or the dialysis nephrologist to try to correct bone metabolism disease in this population is worthy of consideration. Additionally, these patients have more severe PAD including small vessel diseases, which preclude normal healing.
When a Charcot reconstruction failure develops, one must consider amputation. Before making this decision, one needs to consider factors including the patient’s potential to be a community ambulator, his or her adherence to recommended treatment and, most especially, the viability of the opposite limb.
It has been the senior author’s experience that in many instances, the salvaged Charcot limb eventually becomes the patient’s only limb when diabetic complications result in contralateral amputation. One needs to recognize that Charcot reconstruction does nothing to reverse the metabolic damage that created the Charcot foot just as bypass and endovascular surgeries do nothing to reverse the patients’ indicated pathology. It should be our goal as surgeons to try to restore function, and provide the patient with an opportunity to ambulate for as long as he or she reasonably can.
We should not delude ourselves with the idea that we are curing anything with these surgeries. However, repair of the Charcot foot can be worthwhile with years of improved ambulation and the quality of life that the freedom of bipedal gait provides our patients.
Dr. Grant is a Fellow of the American College of Foot and Ankle Surgeons, and is board-certified by the American Board of Podiatric Surgery. He is an instructor in the Department of Surgery at Eastern Virginia Medical School and is in private practice in Virginia Beach, Va.
Ms. Grant is a fourth-year podiatric medical student at the College of Podiatric Medicine and Surgery at Des Moines Medical University.
Mr. Barbato is a graduate of James Madison University and a current applicant to colleges of podiatric medicine.
1. Stapleton J, Belczyk R, Zgonis T. Revisional Charcot foot and ankle surgery. Clinics Podiatr Med. 2009; 26(1):127-39.
2. Frykberg RG, Zgonis T, Armstrong DG, et al. Diabetic foot disorders: a clinical practice guideline. J Foot Ankle Surg. 2006; 45(5):1-66.
3. Shapiro SA, Stansberry KB, Hill MA, Meyer MD, McNitt PM, Bhatt BA, Vinik AI. Normal blood flow response and vasomotion in the diabetic Charcot foot. J Diabetes Complications. 1998; 12(3):147-53
4. Palena LM, Brocco E, Manzi M. Critical limb ischemia in association with Charcot neuroarthropathy: complex endovascular therapy for limb salvage. Cardiovasc Intervent Radiol. 2013; (Epub ahead of print)
5. Palena LM, Brocco E, Ninkovic S, Volpe A, Manzi M. Ischemic Charcot foot: different disease with different treatment? J Cardiovasc Surg (Torino). 2013;54(5):561-6
6. Grant WP, Rubin LG, Pupp GR, Vito G, Jacobus D, Jerlin E, Tam HS. Mechanical testing of seven fixation methods for generation of compression across a midtarsal osteotomy: a comparison of internal nd external fixation devices. J Foot Ankle Surg. 2007; 46(5):325-35.
7. Cooper PS. Application of external fixators for management of Charcot deformities of the foot and ankle. Foot Ankle Clin. 2002; 7(1):207–254.
8. Pinzur MS, Gil J, Belmares J. Treatment of osteomyelitis in Charcot foot with single-stage resection of infection, correction of deformity, and maintenance with ring fixation. Foot Ankle Int. 2012; 33(12):1069-74.
Editor’s note: For further reading, see “Limb Salvage And The Charcot Foot: What The Evidence Shows” in the March 2011 issue of Podiatry Today, “Emerging Concepts In Fixation For Charcot Midfoot Reconstruction” in the February 2011 issue or “Current Concepts With External Fixation And The Charcot Foot” in the October 2013 issue.
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