Managing Ulcers On The Charcot Foot

Neuropathic osteoarthropathy, or Charcot arthropathy, is a condition associated with a loss of sensory nerve function and concurrent vascular dynamic changes. In the acute setting, Charcot can result in bone and joint deformation and fragmentation. If it is not treated early and aggressively, the collapse of involved joints will cause instability, deformity and subject bony prominences to ulceration and infection.
The incidence in the United States and internationally of those with diabetes who have Charcot arthropathy ranges from 7.5 to 13 percent. Internationally, 10 to 20 percent of those with tabes dorsalis and 20 to 25 percent of patients with syringomyelia have some degree of Charcot arthropathy. The age of onset is usually between the fourth and fifth decade with a diagnosed duration of diabetes greater than 15 years. Presentation is usually unilateral but bilateral involvement has been noted at 5.9 to 39.3 percent. Ethnic groups are equally susceptible to having a Charcot arthropathic event.

Understanding The Etiology Of Charcot Arthropathy
Two independent theories, the “neurotraumatic” and the “neurovascular” theories, have been proposed as to the cause of this deformity. However, the consensus of current literature indicates a combination of factors from both theories is generally present in Charcot arthropathy.

The neurotraumatic theory (German theory) proposes that an unperceived trauma to an insensate foot renders the patient unaware of osseous destruction that occurs during ambulation. The resulting trauma leads to progressive destruction and significant damage to bone and joints.
The neurovascular theory (French theory) proposes that autonomic neuropathy, caused by the underlying nervous system impairment and degeneration, results in hyperemic demineralization that leads to osteopenia. The combination of these theories with initial abnormal bone formation due to autonomic deformity and the following microtrauma of the insensate foot, results in multiple fractures and joint subluxation.
Shapiro, et. al., (1988) concluded blood flow in Charcot patients is intact and loss of blood flow in patients with diabetes is protective against Charcot. While this may be worthy of further investigation, our clinical experience has demonstrated significant limb ischemia in the face of chronic Charcot. While blood flow may have been intact at the time of the initial Charcot episode, it may be deficient several years later when treating the chronic Charcot foot deformity. This is of particular importance when evaluating the non-healing Charcot ulceration and also in considering surgical alternatives in the management of this patient population.

Key Clinical Signs And Symptoms
The clinical presentation of Charcot arthropathy generally begins with inflammation, localized warmth to extremity (3 to 7ºF when compared to the non-affected foot or otherwise normal skin temperature), diffuse erythema, joint effusion, intact skin without ulceration and loss of protective sensation. Up to 75 percent of acute Charcot arthropathy patients will present with some level of pain. However, many present with no pain or pain that is significantly less than expected when one considers the clinical and radiographic findings. These patients may have instability, deformity and loss of joint function. In extreme cases, the foot may present as a “loose bag of bones.” Approximately 40 percent of Charcot arthropathy patients have a concomitant ulceration, thereby complicating the diagnosis and raising concern for osteomyelitis.¹

Eichenholtz described the staging of Charcot arthropathy, which is based on clinical and radiographic changes that progress from the acute phase through the healing phase (calescence) to the resolution phase. One should use radiographs to stage the disease and monitor its progression. In the acute or active stage, you will see persistent or progressive joint effusion, narrowing of the joint space, soft tissue calcification, minimal subluxation, preservation of bone density (unless infected) and fragmentation of eburnated subchondral bone. This is often followed by progressive destruction of articular surfaces, subchondral sclerosis, osteophytosis, intraarticular loose bodies, continued subluxation and fracture/dislocation of the bony architecture.
The healing or coalescent stage is observed with serial radiographs that show absorption of fine debris, periosteal new bone formation, fusion of bone fragments, exuberant bone growth, decreased joint mobility, increased stabilization, increased bone density and sclerosis with remaining deformity.
The remodeling (reconstructive) stage is significant for repair, consolidation and healing allowing for increased stability with remodeling and ankylosis.²

Ancillary Diagnostic Methods You Need To Know
There are some optional procedures that can be helpful when diagnosing Charcot. You can use bone scintigraphy when you are unable to differentiate between osteomyelitis and Charcot. Clinical diagnosis can be a dilemma when a patient presents with a chronic non-healing ulceration secondary to a Charcot deformity. Is the ulceration simply due to the increased pressure of the bony deformity or is there underlying osteomyelitis? This is often difficult to assess using clinical and plain film radiography alone. Confirmatory diagnosis methods can meet with some ambiguity and debate, but there are more tests available now that may suit your particular patient situation.
Indium-111 white blood cell scan is more specific than technetium-99 and gallium-67 scans. When positive in the very late phases (up to 24 hours), Indium-111 WBC scans can be used to confirm a diagnosis of osteomyelitis.
MRI may be useful in distinguishing between osteomyelitis and Charcot but the sensitivity and specificity are often dependent on the radiologist’s technical skill. Generally, obtaining a MRI can be helpful for surgical planning as it allows you to assess the proximal extent of possible bone infection.
Bone biopsy remains the gold standard for identifying osteomyelitis and differentiating Charcot arthropathy. A microscopic analysis of osteomyelitis will reveal an eroded bone architecture and a field filled with leukocytes. In the case of Charcot arthropathy, a synovial biopsy identifies small fragments of bone and cartilage debris that are embedded in the synovium due to joint destruction rather than infection.

How To Differentiate Between Charcot And Osteomyelitis
Open ulceration in a neuropathic foot always necessitates careful evaluation to ensure a correct diagnosis and to prevent unnecessary amputation. Clinical presentation of an active Charcot event with erythema, swelling and increased warmth can appear very similar to an infection. When the clinical presentation lacks ulceration, a point of entry or an abscess, the patient most likely is in the early active stages of Charcot arthropathy. However, in the face of a chronic ulceration that presents with concurrent extremity redness, edema and calor, you must carefully scrutinize your clinical suspicion of osteomyelitis.

Ulcerations with an apparently healthy wound base, no evidence of bone exposure and indefinite radiographic findings may require serial radiographs and ancillary studies, such as a bone scan or bone biopsy, to aid you in the decision-making processes. Bone imaging is extremely sensitive for bone pathology but it is often less specific and inconclusive. Technetium-99 is effective for localizing the area of bone involved but it is often insufficient to completely differentiate between Charcot and osteomyelitis.
Indium-111 imaging has an overall sensitivity of 90 percent and a specificity of 95 percent for detecting an abscess. However, when the literature reviewed is focused on the ability of Indium testing to differentiate the causative pathology, the sensitivity is noted to range from 62 to 98 percent for osteomyelitis. Often, one may employ a combination of imaging techniques to localize the activity and identify osteomyelitis versus Charcot arthropathy. Keep in mind that chronic osteomyelitis is noted to have a lower sensitivity for Indium-111 imaging and clinical follow-up is essential.³
Lab studies can aid with the clinical diagnosis and differentiation of Charcot arthropathy versus osteomyelitis but there is significant ambiguity. White blood cell count (WBC) with differential will be elevated with a left shift when infection is present, but WBC can also be a marker for inflammation and may be moderately elevated in Charcot arthropathy. To add to this complex situation, not all people with diabetes are able to mount a significant immune response to infection. Therefore, they may have normal appearing WBC levels in the face of abscess/osteomyelitis.

Erythrocyte sedimentation rate (ESR) is elevated in infection and is also a nonspecific marker for inflammation. Significantly increased ESR>70 is highly predictive of osteomyelitis.⁴ Glycosylated hemoglobin indicates the level of hyperglycemic control. Hyperglycemia causes nonenzymatic collagen glycosylation, which can lead to laxity in ligaments and unstable joints as well as neuropathy. In non-diabetics, obtaining B-12/folate deficiency and liver function tests may be necessary to rule out peripheral neuropathy as a result of chronic alcoholism.

A Guide To Conservative Treatment Options
When you seek to treat a patient conservatively, you have numerous options. Total contact casting (TCC) is the gold standard of conservative treatment for immobilizing, offloading and supporting the structure of the foot until the acute stage of Charcot arthropathy resolves. Ideally, one should combine a TCC with complete non-weightbearing (NWB) of the affected extremity but NWB status is often difficult to obtain in this patient population due to concurrent obesity, visual impairment and upper extremity weakness. Patients unable to comply with NWB status will have a longer healing time and risk further deformity and ulceration. When using TCC, be aware that the modality requires weekly cast changes for three to six months with regular debridement of pre-ulcerative or ulcerative lesions.
Alternative devices that can assist in partial non-weightbearing include the removable cast walkers, patellar tendon-bearing brace, accommodative footwear with a modified AFO, a Charcot restraint walker (CROW) and double upright AFO.

Obtain serial radiographs monthly to evaluate progression. Discontining offloading is dependent on clinical, radiographic and dermal thermometric signs of quiescence. In our practice, we generally combine a return to weightbearing status with progression into a removable cast walker device for two to three weeks. Subsequently, we emphasize appropriate prescriptive shoewear, including custom molded shoes, extra depth with plastazote insoles and steel shank shoes with a rocker bottom if the patient has an ulceration. Long-term management requires life-long protection of the involved extremity or possible surgical intervention to establish a stable weightbearing platform.

Pearls For Surgical Treatment
Goals of surgical treatment include correction of the deformity, which prevents the foot from being protected appropriately in accommodative shoewear. In addition, seek to create a stable plantigrade foot that allows for ambulation and minimizes the risk for ulceration.

Surgical procedures are often indicated for reulceration, misaligned, unstable or nonreducible fractures or dislocations that fail to resolve with conservative care. A study by Armstrong, et. al., found that of 55 patients initially treated with conservative care, 25 percent eventually underwent corrective surgery. Two-thirds required plantar exostectomies and one-third required some degree of joint fusion.¹
Is active inflammation a contraindication for surgical correction? Depending on the location and severity of the deformity, surgical treatment can vary from exostectomy, osteotomy, arthrodesis, arthroplasty, open reduction and internal fixation to tendon lengthening procedures and more. In the face of forefoot deformities, patients with bony prominences or recurrent ulcerations may need resectional arthroplasties, metatarsal head resections or cheilectomies.

Pertinent Points On Performing An Exostectomy
Exostectomy is indicated for relatively inactive, sedentary patients with recurrent ulceration secondary to a bony prominence with a rocker bottom deformity.
The procedure is relatively simple, beginning with a long elliptical incision, which often includes excision of the ulceration. One would resect the bony prominence through this incision with an osteotome, resulting in a convexity in the bone. Proceed to do a primary closure of the incision and allow for weightbearing in three to six weeks even in the face of most plantar incision sites. Complications include “chasing the bump” or an over-aggressive bone resection that results in an unstable foot and risk for further collapse.

A retrospective study of 27 exostectomy procedures found 74 percent achieved resolution of plantar ulceration. The study also noted a higher complication rate when addressing lateral Charcot pathology (six of the seven complications found), contrasting procedures that addressed medial bone pathology.⁵ Rosenblum, et. al., performed a retrospective study of 32 lateral column procedures with a success rate of 89 percent. Eight patients required revisional surgery.⁶

What About Reconstruction And Arthrodesis Procedures?
Reconstruction and arthrodesis procedures of the mid- and rearfoot offer a better long-term outcome. However, due to the extensive nature of the procedure and demands of the postoperative period, proper patient selection is imperative.
Postoperatively, patients generally must maintain a non-weightbearing status for a lengthy period of time, often five to six months. One may employ bone grafts as well as screws, plates, intermedullary rods and percutaneous fixation, including external fixation devices. For midfoot deformities, correcting a rocker-bottom deformity may require midfoot fusion, medial column fusion, osteotomies and excising a portion of the mid-tarsus. Charcot involving dystrophy of the ankle may require open reduction and internal fixation, arthrodesis, talectomy or other aggressive realignment procedures.
Complications include delayed union, nonunion, fixation failure, ulceration, infection, reactivation of Charcot arthropathy, further deformity, the need for revisional surgery and the need for an amputation of the extremity. The patient must enter into the process of Charcot reconstruction with the understanding that it is essentially a limb salvage procedure and the risk concern for complications (including amputation) is very high.
Often equinus deformity can cause or exacerbate Charcot arthropathy. A tight Achilles tendon resulting from weak dorsiflexors or tendon glycosilation can increase the stress over the tarsometatarsal, naviculocuneiform and midtarsal joints. The deforming force can cause joint collapse in multiple planes and increase forefoot pressures, which may elevate the risk of ulcerations and recurrent ulceration.

In Conclusion
More favorable outcomes in the face of Charcot arthropathy are noted when there is early/immediate diagnosis and aggressive management. Treatment of concurrent ulceration in Charcot arthropathy includes offloading, immobilization, debridement and local care. Ulcer treatment for the Charcot patient is very much the same as that which would be employed in the non-Charcot neuropathic diabetic foot ulceration. One should consider aggressive use of bioengineered tissues and other advanced healing modalities early in the treatment course due to the high risk of these particular ulcerations.
Ruling out underlying infection/osteomyelitis is more complicated in the ulceration due to Charcot but one should employ advanced imaging techniques and bone biopsy in the face of an uncertain clinical scenario. In cases in which offloading and local care for Charcot arthropathy/ulceration is not successful and re-ulceration and worsening of the deformity is present, consider surgical intervention through exostectomy or other reconstructive procedures to provide the best long-term outcome.
In the Charcot foot, it is imperative to address the underlying etiology when possible. Ulceration in Charcot can usually be directly attributed to a resultant deformity or a malalignment affecting the plantar weightbearing surface. In the ideal scenario, the active ulceration would first be healed with offloading, debridement and local management. Once you have achieved a closed skin envelope, you can perform the appropriate surgical procedures to address the causative factors and prevent ulcer recurrence. In this manner, one can minimize surgical complications of wound infection and dehiscence.

Dr. Steinberg is an Assistant Professor in the Department of Orthopaedics/Podiatry Service at the University of Texas Health Science Center in San Antonio, Texas. He is a Fellow of the American College of Foot and Ankle Surgeons.
Dr. Jensen is a second-year resident at the University of Texas Health Science Center in San Antonio, Texas.

CE Exam #110

Choose the single best response to each question listed below:

1. What was the most common cause of Charcot in the 1800s?
a) diabetes
b) pneumonia
c) osteomyelitis
d) syphilis

2. Which of the following is the least common modern cause of Charcot arthropathy?
a) diabetes
b) tabes dorsalis
c) pneumonia
d) syringomyelia

3. Charcot most commonly presents in which of the following patterns?
a) upper extremity, unilaterally
b) lower extremity, unilaterally
c) upper extremity, bilaterally
d) lower extremity, bilaterally

4. Which of the following are the two most commonly accepted theories which describe the pathophysiology of Charcot?
a) ischemic and neuromuscular
b) neuromuscular and neurovascular
c) infectious and neurotraumatic
d) neurotraumatic and neurovascular

5. Increased temperature in an extremity can be a clinical finding in Charcot. How many degrees of temperature difference is typically noted in an active Charcot extremity when compared to the unaffected limb?
a) 1-2º F
b) 3-7º F
c) 15-20º F
d) 22-30º F

6. Which of the following is the “gold standard” for differentiating Charcot from osteomyelitis?
a) indium-111
b) technetium-99
c) WBC with differential
d) bone biopsy

7. Which of the following is the “gold standard” for offloading the acute Charcot ulceration?
a) total contact cast
b) removable cast walker
c) CROW walker
d) custom molded shoe

8. Equinus is problematic in the face of Charcot arthropathy because it …
a) produces increased plantar forefoot pressures
b) can cause midtarsal joint stress and collapse
c) increases ulceration risk
d) all of the above

9. Which of the following describes a complication directly related to overaggressive bone resection when performing an exostectomy in the Charcot foot?
a) destabilization of the remaining joints
b) infection
c) dehiscence
d) gangrene

10. According to Eichenholtz, which of the following stages of Charcot is described by “progressive joint effusion, narrowing of the joint space, soft tissue calcification and joint subluxation”?
a) remodeling
b) coalescence
c) reconstruction
d) acute

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References:

References
1. Armstrong DG, et. al.. The Natural History of Acute Charcot’s Arthropathy in a Diabetic Foot Specialty Clinic, Diabetic Medicine, Vol 14, 1997
2. Sanders LJ, Frykberg RG: Diabetic neuropathic osteoarthropathy: The Charcot Foot, New York, 1991.
3. Splittgerberger GF, Spiegelhoff DR, and Buggy BP. Combined Leukocyte and Bone Imaging Used to Evaluate Diabetic Osteoarthropathy and Osteomyelitis, Clinical Nuclear Medicine, Vol. 3, March 1989
4. Keleta JL, Fleischli JW, Reilly CH. The Diagnosis of Osteomyelitis in Diabetes Using Erythrocyte Sedimentation Rate: A Pilot Study. JAPMA, Vol. 91:445-450, 2001.
5. Catanzariti AR, Mendicino R, and Haverstock B. Ostectomy for Diabetic Neuroarthropathy Involving the Midfoot, Journal of Foot and Ankle Surgery, Vol. 39 No. 5, September/October 2000
6. Rosenblum BI, et al. Neuropathic Ulcerations: Plantar to the Lateral Column in Patients with Charcot Foot Deformity: A Flexible Approach to Limb Salvage, Journal of Foot and Ankle Surgery, Vol.36 No.5, 1997.