When performing the Scandinavian Total Ankle Replacement (STAR), the positioning of the talar component and the selection of mobile-bearing thickness are critical. A biomechanical experiment was undertaken to establish the effects of these variables on the range of movement (ROM) of the ankle. Six cadaver ankles containing a specially-modified STAR prosthesis were subjected to ROM determination, under weight-bearing conditions, while monitoring the strain in the peri-ankle ligaments. Each specimen was tested with the talar component positions in neutral, as well as 3 and 6 mm of anterior and posterior displacement. The sequence was repeated with an anatomical bearing thickness, as well as at 2 mm reduced and increased thicknesses. The movement limits were defined as 10% strain in any ligament, bearing lift-off from the talar component or limitations of the hardware. Both anterior talar component displacement and bearing thickness reduction caused a decrease in plantar flexion, which was associated with bearing lift-off. With increased bearing thickness, posterior displacement of the talar component decreased plantar flexion, whereas anterior displacement decreased
We assessed peripheral nerve function during and after lower-limb lengthening by callotasis in 14 patients with short stature, using motor conduction studies. Four patients with short stature of varying aetiology showed unilateral and one showed bilateral weakness of foot
We have studied the relationship between movements of the foot and ankle and venous blood flow from the lower limb using colourflow Duplex ultrasound to determine the optimum type of exercise for promoting venous return. Studies of both active and passive movements were carried out on 40 limbs in 20 subjects (18 men; 2 women), with a median age of 27 years (20 to 54). We assessed ankle
Thrombin has many biological properties similar to those of growth factors. In a previous study, we showed that thrombin improves healing of the rat tendo Achillis. Low molecular weight heparin (LMWH) inhibits the activity and the generation of thrombin. We therefore considered that LMWH at a thromboprophylactic dose might inhibit tendon repair. Transection of the tendo Achillis was carried out in 86 rats and the healing tested mechanically. Low molecular weight heparin (dalateparin) was either injected a few minutes before the operation and then given continuously with an osmotic mini pump for seven days, or given as one injection before the operation. In another experiment ,we gave LMWH or a placebo by injection twice daily. The anti-factor Xa activity was analysed. Continuous treatment with LMWH impaired tendon healing. After seven days, this treatment caused a 33% reduction in force at failure, a 20% reduction in stiffness and a 67% reduction in energy uptake. However, if injected twice daily, LMWH had no effect on tendon healing. Anti-factor Xa activity was increased by LMWH treatment, but was normal between intermittent injections. Low molecular weight heparin delays tendon repair if given continuously, but not if injected intermittently, probably because the anti-factor Xa activity between injections returns to normal, allowing sufficient thrombin stimulation for repair. These findings indicate the need for caution in the assessment of long-acting thrombin and factor Xa inhibitors.
A cavovarus foot deformity was simulated in cadaver specimens by inserting metallic wedges of 15° and 30° dorsally into the first tarsometatarsal joint. Sensors in the ankle joint recorded static tibiotalar pressure distribution at physiological load. The peak pressure increased significantly from neutral alignment to the 30° cavus deformity, and the centre of force migrated medially. The anterior migration of the centre of force was significant for both the 15° (repeated measures analysis of variance (ANOVA), p = 0.021) and the 30° (repeated measures ANOVA, p = 0.007) cavus deformity. Differences in ligament laxity did not influence the peak pressure. These findings support the hypothesis that the cavovarus foot deformity causes an increase in anteromedial ankle joint pressure leading to anteromedial arthrosis in the long term, even in the absence of lateral hindfoot instability.