The effect of active toe movement (AToM) on asymptomatic deep vein thrombosis in patients with acute foot and ankle injury treated with cast - a prospective randomised controlled trial
B. Hickey, R. Alikhan, A. Cleves, N. Pugh, L. Nokes, A. Perera
Introduction: Patients with lower limb trauma and cast treatment are at risk of venous thromboembolism (VTE). Active toe movement reduces venous stasis with a below knee cast in situ, which may influence rates of deep vein thrombosis (DVT). Our aim was to determine the effect of an active toe movement protocol (AToM) on asymptomatic DVT rates in patients with acute foot and ankle trauma treated with below knee cast.
Methods: In this prospective randomized controlled study, 100 adult patients with acute foot or ankle trauma treated with below knee cast were recruited at the University Hospital of Wales. In accordance with NICE guidance, all patients were assessed for risk of VTE. If patients had permanent risk factors for VTE they were ineligible for the study and provided with low molecular weigh heparin thromboprophylaxis. After enrolment, patients who were randomized to AToM were advised to perform regular daily toe movement exercises according to a defined protocol. On discharge from fracture clinic all patients underwent bilateral lower limb venous ultrasound to identify DVT.
Results: 78 patients of mean age 36 years (range 16-60) completed the study. 65% (n=51) were male. 59% (n=46) of patients were treated with cast for ankle fractures. 21 (27%) patients were found to have deep vein thrombosis on ultrasound examination. All of these occurred in the lower limb that had been injured and treated in cast. The DVT rate was 13/39 (33.3%) in intervention group and 8/39 (20.5%) in control group. These differences were not statistically significant (p=0.202).
Conclusions: Although venous stasis may be reduced by performing regular active toe movements with a below knee cast in situ, this does not appear to influence rates of DVT. Local endothelial dysfunction due to trauma may influence the pathogenesis of DVT to a greater extent than venous stasis.
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