Emerging Concepts In Fixation For Charcot Midfoot Reconstruction

Volume 24 - Issue 2 - February 2011
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What The Literature Reveals About The Incidence And Etiology Of Charcot Neuroarthropathy

Several population-based studies have indicated that the incidence of the Charcot deformity ranges from 0.10 percent to 2.9 percent.^1-3 In a controlled study of 680 patients with diabetes, 0.15 percent developed Charcot foot deformity.⁴ In an observational study, Fibrin and colleagues reported an incidence of 0.03 percent in 3,000 patients with diabetes.⁵ The incidence is undoubtedly greater because many cases are not reported and there are few long-term studies that monitor the occurrence, development and frequency of the Charcot deformity in the diabetic population.

With the dramatic increase in people developing diabetes, there will be an increase in Charcot neuroarthropathy. The most significant predisposing factor in the development of the Charcot deformity is neuropathy. Between 9 to 32 percent of patients with diabetes have decreased sensation of there lower extremities.⁶ Researchers have also determined that pronounced neuropathy was the constant factor in the Charcot foot rather than the length of time that the patient had diabetes or how well the patient’s diabetes was controlled.⁷

Charcot patients usually do not report a history of trauma. Most indicate that their foot just became red and swollen, and the shape of their foot seemed to change. Some patients report pain but many have no significant discomfort.

One theory as to the Charcot pathogenesis is that any form of trauma may initiate the process. This can be acute, sub-acute or repetitive. Just walking with a loss of the protective threshold can start the process. Weightbearing results in microfractures initially but with continued walking, the fractures become more severe and fragmentation occurs with eventual collapse and deformity of the foot.

Over a period of weeks and months, the reparative process creates callus formation that radiographically resembles a hypertrophic nonunion. This process is known as the neurotramautic theory. The neurovascular concept suggests that a state of hyperemia exists from an overactive vasomotor autonomic neuropathy. Increased blood flow to the lower extremity increases local bone metabolism. This in turn stimulates osteoclastic activity, resulting in resorption of bone. The developing osteopenia weakens the bone, predisposing it to failure.^8-10 Pinsur feels that the pathogenesis of Charcot neuropathy may actually involve a combination of both processes.¹¹

When peripheral neuropathy results in a loss of sensation and a loss of motor function, this creates an imbalance of the intrinsic musculature of the foot. As the Achilles tendon continues to contract, this creates excessive stress through the midfoot, which results in collapse of the arch and development of a rocker bottom deformity.

References

1. Rajbhandari SM, Jenkins RC, Davies C, et al. Charcot neuroarthropathy in diabetes mellitus. Diabetologia 2002;45(8):1085-96.

2. Sanders LF: Charcot neuroarthrophy of the foot. In: Bowker J, Pfeifer M (eds): The Diabetic Foot, 6th edition. Mosby, St. Louis, 2001, p. 439-66.

3. Cofield RH, Motrisin M, Beabout JW. Diabetic neuroarthropathy in the foot: patient characteristics and patterns of radiographic changes. Foot Ankle Int. 1983;4(1):15-22.

4. Sinha S, Munichoodappa CS, Kozak G. Neuro-arthropathy (Charcot joints) in diabetes mellitus (clinical study of 101 cases). Medicine 1971;51(3):191-210.

5. Fabrin J, Larsen K, Holstein P. Long-term follow-up in diabetic Charcot feet with spontaneous onset. Diabetes Care 2000;23(6):796-800.

6. Pakarinen T, Laine HJ, Honokonen SE, et al. Charcot arthropathy of the diabetic foot. Current concepts and review of 36 cases. Scand J Surg 2002; 91(2):195-201.

7. Foltz K, Fallat L, Schwartz, S. Usefulness of a brief assessment battery for early detection of Charcot foot deformity in patients with diabetes. J Foot Ankle Surg 2004; 43(2): 87-92.

8. Herbst SA, Jones KB, Saltzman CL. Pattern of diabetic neuropathic arthropathy associated with the peripheral bone mineral density. J. Bone Joint Surg. 2004:86(3):378-383.

9. Young M, Breddy JL, Vevers A, et al. The prediction of diabetic peripheral neuropathy using vibration perception thresholds: a prospective study. Diabetes Care. 1994:17(6):557-560.

10. Young MJ, Marshall A, Adams, JE, et al. Osteopenia, neurological dysfunction, and the development of Charcot neuroarthropathy. Diabetes Care 1995;18(1): 34-38.

11. Pinzur MS. Current concepts review: Charcot arthropathy of the foot and ankle. Foot Ankle Int. 2007:28(8):952-959.

Author(s):

Lawrence M. Fallat, DPM, FACFAS

Given the challenges with reconstructive surgery for patients with Charcot neuroarthropathy, this author reviews the different fixation options and offers step-by-step pearls on the use of intramedullary screw fixation.

Charcot neuroarthropathy is a dynamic non-infectious destructive process, which can affect the bones and joints of the foot and the ankle. Diabetes with pronounced neuropathy is the most common etiology of this condition but any neuromuscular disorder that damages the peripheral nerves can result in Charcot foot pathology.

This includes multiple sclerosis, syringomyelia, cerebral palsy and Charcot-Marie-Tooth disease. Other conditions such as leprosy, syphilis and rheumatoid arthritis can also result in Charcot neuroarthropathy. Trauma to the peripheral nerves and prolonged exposure to toxic substances such as alcohol can also result in Charcot neuroarthropathy.

The basic goal for surgery of the deformed Charcot foot is to create a stable, braceable, plantigrade foot. One can accomplish this by correcting the foot deformity through wedging osteotomies, removing bony prominences and performing an arthrodesis. Surgery should result in no pressure points on the foot and should prevent amputation.

Key Insights On ‘Superconstructs’

In 2009, Sammarco developed the concept of “superconstructs” to describe the use of surgical techniques when the normal principles of internal fixation are abandoned to reduce the likelihood of failure of the procedure.¹

Superconstructs are defined as follows:

1) fusion that extends beyond the zone of injury to include joints that are not affected to improve fixation;
2) bone resection performed to shorten the extremity to allow for adequate reduction of the deformity without undue tension on the soft tissue envelope;
3) use of the strongest fixation device that can be tolerated by the soft tissue envelope; and
4) application of the fixation devices in a position that maximizes mechanical function.

Surgeons use superconstructs in situations in which they expect technical problems in achieving a successful outcome and in patients with bone loss, dysvascular bone, severe osteoporosis and major deformity correction. Podiatric surgeons may also use these superconstructs when patients have comorbidities that would adversely affect healing.

Assessing The Pros And Cons Of Plantar Plating And Locking Plates

Surgical reconstruction with fixation of the neuropathic Charcot foot deformity can be difficult and challenging to the surgeon. In addition to correcting a severe foot deformity, the bone is usually of poor quality and the ability to heal may be impaired.

The bone may be fragmented and unable to hold a screw. When you combine this with premature ambulation, it can result in a loss of fixation and correction. Even with stable fixation, the incision site may be prone to dehiscense, ulceration, infection and osteomyelitis, which could further weaken the bone.

Current fixation options for the Charcot foot include plantar plating, locking plates, external fixation and intramedullary screws.