Abstract
Syndesmotic ankle sprains, i.e. injuries to the distal tibiofibular syndesmosis, are debilitating injuries often associated with arduous rehabilitation and recovery. External foot rotation, induced by internal rotation of the tibia, is hypothesized as the primary mechanism of these injuries, but the role of ankle flexion remains poorly understood for both injury patterns and tolerances. Furthermore, clinical observations include combinations of ligament and osseous injuries, with unclear links between causation and injury patterns.
The main objective of this thesis was to determine the injury pattern and sequence of ankle ligaments during excessive external foot rotation in varying ankle flexion postures: neutral, dorsiflexed (15°), and plantarflexed (30°). Specifically, this thesis aimed to address deficiencies in the literature by improving boundary conditions in experiments testing forceful external foot rotation in cadavers. Furthermore, this thesis aimed to determine an injury occurrence interval for syndesmotic ankle sprains, relative to the leg kinematic input of external foot rotation, in a neutral flexion posture. Changes in this injury interval were considered for varying flexion postures.
Nine matched-pair legs from non-senescent (47 ± 11.3 yrs.), large (94.4 ± 30.9 kg, 178.1 ± 5.9 cm) male cadaver legs were disarticulated at the knee joint. The proximal tibia was fixed and the fibula left unconstrained. External foot rotation was imposed by internally rotating the tibia while motion of the calcaneus and first metatarsal head were constrained. A nominal preload of 2 kN was imposed along the tibia long-axis. Osteoligamentous injury timing was determined from acoustic sensors, strain gauges, force/moment measurements, and three-dimensional bony kinematics as external foot rotation, defined as calcaneus yaw relative to the tibia long-axis, was applied. Post-test necropsies were performed to identify injuries.
In neutral, syndesmotic injuries were identified in five of nine legs and deltoid injuries in nine of nine legs. Plantarflexion was protective of the syndesmotic ligaments, such that zero of four specimens sustained syndesmotic injury, yet three of four sustained a deltoid injury. Dorsiflexion focused loading through the syndesmosis during external rotation, such that four of four specimens sustained a syndesmotic injury and three of four a deltoid injury. As external rotation is applied, the talus creates lateral and posterior tibiofibular diastasis, eventually disrupting the syndesmotic ligaments. When legs are in neutral or dorsiflexion, this is exaggerated, yet protected against when combined with plantarflexion. This indicates plantarflexion does not widen the ankle mortise in the same way as in dorsiflexion or neutral, even under the same applied preload and external rotation.
These injury pattern and incidence results will inform future clinical diagnosis, care, and rehabilitation techniques for syndesmotic ankle sprains. Bone kinematic interactions and injury propagation and occurrence data will be used to validate a finite element ankle surrogate model. Ultimately, this model will act a design tool for assessing future countermeasures aimed at mitigating syndesmotic ankle sprains.
