Go to Top

Complications with Charcot Foot

CharcotFoot1

The Charcot foot normally goes unrecognized, especially during the acute phase, until further complications are observed. Early detection and diagnoses, instant immobilization, and a lifelong regimen of preventive care can significantly minimize the morbidity that normally comes with this possibly devastating diabetic neuropathic condition. If undetected and inaccurately recognized or inappropriately managed, the Charcot foot can have dreadful consequences, unfortunately including amputation.

In the acute phase, the Charcot foot is normally painless and may appear like deep venous thrombosis or cellulitis. Although the first radiograph may come out normal, making accurate diagnosis difficult, instant detection and immobilization of the foot is crucial in the Charcot foot management. A lifelong plan of patient education, protective footwear, and foot care regimen is necessary for the efficient prevention of complications including ulceration of the foot.

Charcot Foot: The Pathogenesis

There are two theories that have been established to explain the pathogenesis of Charcot foot—the neurotraumatic theory and the neurovascular theory. The former points to the bony damages to the proprioception and loss of pain coupled with mechanical and repetitive trauma to the foot. The latter, on the other hand, postulates that damages to the joint is secondary to vascular reflex that is autonomically stimulated brings about periarticular osteopenia and hyperemia coupled with contributory trauma. Inherent muscle imbalance and increased plantar and heel forces result in eccentric loading of the foot, inducing ligament laxity, microfractures, and progression that ultimately causes bony destruction.

As much as 50% of Charcot foot patients recall a minor precipitating traumatic event like a previous foot procedure or an ankle sprain; however, several cases of Charcot joint changes, including those with foot inflammations, believe that hyperemia is the cause.

Charcot Foot: The Orthotic Management

Treatment of Charcot foot is primarily aimed at offloading the foot, treating the bone disease, and the elimination of the likely occurrence of further foot fractures. Because of the many etiologies of increased bone resorption or secondary osteoporosis in Charcot foot patients and minimal randomized placebo-controlled examinations and tests in this area, treatment methodologies are largely based on professional advice instead of the highest levels of evidence from clinical cases.

As soon as the disease is evaluated and diagnosed to be on its active stage, the patient is immediately and strictly protected from excess weight-bearing. In severe cases, especially those with bilateral involvement, bed rest is always advised. Patients who are more agile and with unilateral involvement fared pretty well on the contralateral foot with crutch-walking. As a rule of thumb, since forefoot lesions get less body weight, they will need less protection. Forefoot fractures that are non-displaced may positively respond to shoes or sandals that are rocker-soled without the full unweighting.

On the other hand, hindfoot lesions require complete non-weight-bearing to avoid destructive deformity during the resorptive phase. It would help to look at treating Charcot foot as analogous to that of Legg-Calve’-Perthes disease of the hip: considerable skeletal deformities will be avoided for as long as the affected joints are immediately placed in proper alignment and weight-bearing factors are held in complete control.

After the end of the active stage, the patients are still however at risk for more pathologic fractures because of the marginal bone density that normally comes with the disease. At this point, the patients are now osteoporotic with the usual lumbering “lead foot” gait of the sensation-less limb increasing the chances of developing more stress fractures.

Charcot foot patients are routinely fit with double upright PTB orthosis complete with adjustable ankles that are attached to a shoe with extra depth and with an accommodative rocker sole, steel shank, and inlay. For more considerably deformed feet, custom-made shoes are required. Recovering Charcot patients are generally required to wear the orthosis for a minimum of one year or until the radiograph results clearly show complete recovery from osteopenia and the achievement of normal levels of bone density.

Because these patients will generally have trouble walking, it is preferred that ankles are not locked against plantarflexion unless there are existing hindfoot problems. It is sometimes useful to use a spring dorsiflexion assist to aid toe clearance or minimize footslap. Here, the rocker sole must be customized since these feet are normally free from ulcers with the weight-bearing restrictions.

As a long-term orthosis method and with a majority of diabetics having volume fluctuations that come secondary to edema, attaching the plastic or metal hybrid brace externally to the shoe is necessary. This allows for the independent adjustment of the shoes, weight-bearing shell, ankle control, and foot orthosis as the patient’s condition slowly improves. As soon as X-ray results show a reconstitution of the bone density, the PTB superstructure is removed, the accommodative foot orthosis and customized shoe continue to provide protection. This orthotic management has successfully prevented the unwanted development of considerable deformities even with the bony destruction presented in radiographs. More than 90% of Charcot cases that have been treated with the above-mentioned method have avoided amputation and developed  ambulatory independency; majority too have been able to successfully discard the PTB orthosis and don only and accommodative rocker sole and foot orthosis.

Summary and Conclusion

Despite the many debates and mysteries behind it, the number of cases on neuropathic arthropathy is believed to grow with the continuing increase in the diabetic’s lifespan. When provided as a part of a comprehensive multi-phase and multidisciplinary treatment methodology, careful orthotic management can remarkably enhance the ambulatory possibility and the quality of life for Charcot foot patients.

 

Resources:

The Charcot Foot in Diabetes: Six Key Points. http://www.aafp.org/afp/1998/0601/p2705.html

Brower  AC, Allman  RM.  Pathogenesis of the neurotrophic joint: neurotraumatic vs. neurovascular.  Radiology.  1981;139:349–54.

Schon  LC, Easley  ME, Weinfeld  SB.  Charcot neuroarthropathy of the foot and ankle.  Clin Orthop.  1998;349:116–31.

Frykberg RG, Eneroth M. Principles of conservative management. In The Diabetic Charcot Foot: Principles and Management. Frykberg RG, Ed. Brooklandville, MD, Data Trace Publishing Company, 2010, p. 93–116

Edmonds ME. The Diabetic Foot: Pathophysiology and Treatment. Clinics in Endicrinology and Metabolism 1986; 15(4) :889-9 16.

Harrelson JM. Management of the diabetic foot. Orthopedic Clinics of North America 1989 ;2t)(4) :605-619.

Titus BR. A patellar-tendon-bearing orthosis. Orthotics and Prosthetics 1975:29(1) :35-40

, ,