Can The Fibula-Pro-Tibia Technique Have An Impact For Diabetic Ankle Fractures?

By Christopher L. Reeves, DPM,Alan A. MacGill, DPM,Amber M. Shane, DPM, and Joseph A. Conte, DPM Clinical Editor: John S. Steinberg, DPM

Ankle fractures in patients with diabetes present a great challenge for the foot and ankle surgeon. Indeed, there is an abundance of literature documenting the difficulty of managing diabetic ankle fractures. Surgical treatment can be fraught with complications such as delayed bone and wound healing, and the development of Charcot neuroarthropathy.

When it comes to treating diabetic ankle fractures, complication rates are high, especially in patients with neuropathy. One reason for this is the altered osteogenesis in patients with diabetes in comparison to that of people without diabetes. In 1988, Loder evaluated the influence of diabetes mellitus on the healing of closed fractures. The study found the overall osseous time to union to be 163 percent longer in the diabetic population. Furthermore, the study found that displaced fractures requiring open reduction internal fixation (ORIF) had a 187 percent longer healing time in patients with diabetes.1

Reddy, et al., studied the mechanical strength of bone in patients with diabetes. The study revealed a 37 percent decrease in maximal load, a 25 percent decrease in deformation and maximal load, and a 38 percent increase in bending stiffness in comparison to patients without diabetes. The authors concluded that diabetic bone was more inflexible and bore decreased loads. Accordingly, they noted that diabetic bone has decreased energy absorbing capacity.2

Cavanaugh, et al. evaluated radiographic abnormalities in patients with diabetic neuropathy. The study demonstrated a substantial number of neuropathic fractures in many of these patients. Moreover, they noted that a significant number of these patients went on to develop Charcot arthropathy.3

An Overview Of The Pathophysiology Of Charcot Arthropathy

Charcot neuroarthropathy is largely associated with longstanding diabetes mellitus. Two main theories exist regarding the development of Charcot joint disease. The first theory, neurotraumatic destruction (also known as the German theory), postulates that the breakdown is a result of cumulative mechanical trauma in a joint that has been rendered insensitive to proprioception and pain.

The joint insult may be major or minor, recognized or unrecognized. Often, when unrecognized microtrauma from abnormal gait causes increased plantar pressure in an insensate limb, this leads to Charcot arthropathy.

The theory of neurovascular destruction hypothesized that a lack of vasomotor tone leads to ligamentous weakening and bone resorption. The neurally stimulated vascular reflex is interpreted as an “autosympathectomy” and eventually induces joint disintegration. While the exact cause of Charcot athropathy is unclear, it is likely that both theories contribute to the pathophysiology of the disease.

Weighing The Various Treatment Options And Potential Complications

The literature shows controversy when it comes to surgical versus non-surgical treatment in this patient population.4-7 McCormack and Leith reported increased infection rates, delayed bone healing and an increased incidence of Charcot joint disease with overall complication rates approaching 47 percent in the surgical treatment of 19 diabetic ankle fractures.8 Bibbo, et al., reported that 5 to 10 percent of all patients with diabetes who sustain an ankle fracture will develop Charcot joint disease.4 More recent studies have shown increases in severe complications, most notably Charcot joint disease and infection, in the non-surgical group.9

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