Diabetes mellitus is considered an indicator of poor prognosis for acute ankle fractures, but this risk may be specific to an identifiable subpopulation. We retrospectively reviewed 42 patients with both diabetes mellitus and an acute, closed, rotational ankle fracture. Patients were individually matched to controls by age, gender, fracture type, and surgical
The relationship between the bone mineral density (BMD) and Charcot arthropathy is unclear. Prospectively, 55 consecutive diabetic patients presenting with a Charcot arthropathy of the foot or ankle were classified as having a fracture, dislocation, or a combination fracture-dislocation pattern of initial destruction. In these groups we used dual-energy x-ray absorptiometry to compare the peripheral bone of the affected and unaffected limbs. The clinical data relating to diabetes and related major comorbidities and the site of the arthropathy (ankle, hindfoot, midfoot, forefoot) were also compared. There were 23 patients with a fracture pattern, 23 with a dislocation pattern, and nine with a combination. The age-adjusted odds ratio for developing a Charcot joint with a fracture pattern as opposed to a dislocation pattern in patients with osteopenia was 9.5 (95% confidence interval 2.4 to 37.4; p = 0.0014). Groups also differed as to the site of the arthropathy. Fracture patterns predominated at the ankle and forefoot whereas dislocations did so in the midfoot. Diabetic Charcot arthropathy of the foot and ankle differs according to the pattern of the initial destruction. The fracture pattern is associated with peripheral deficiency of BMD. The dislocation pattern is associated with a normal BMD.
Previous dye-infusion experiments on cadavers have suggested that the hindfoot should be divided into four muscle compartments including a newly described ‘calcaneal’ element containing quadratus plantae. Since there are no clinical data to support this proposed division, we re-examined the validity of the infusion experiment. We made infusions of dilute Omnipaque at a constant rate into flexor digitorum brevis of four cadaver feet. We monitored the spread of the infusate by real-time CT imaging and measured the pressures at the infusion site by side-ported needles. In all feet, the barrier between flexor digitorum brevis and quadratus plantae became incompetent at pressures of less than 10 mmHg. Pressure gradients in this range cannot be expected to affect tissue perfusion significantly and independently generate compartment syndromes. These results do not confirm those of previous studies carried out by uncontrolled and unmonitored injections made by hand. Injection studies in cadaver limbs can give dramatically different results depending upon the assumptions made when designing the experiment. The technique cannot adequately act as a model of the physiology of the compartment syndrome. As the existence of a physiologically significant compartmental boundary between flexor digitorum brevis and quadratus plantae is based solely on a cadaver infusion experiment the presence of a ‘calcaneal’ compartment has not been confirmed.