In this work, we propose a new quantitative way of evaluating acute compartment syndrome (ACS) by dynamic mechanical assessment of soft tissue changes. First, we have developed an animal model of ACS to replicate the physiological changes during the condition. Secondly, we have developed a mechanical assessment tool for quantitative pre-clinical assessment of ACS. Our hand-held indentation device provides an accurate method for investigations into the local dynamic mechanical properties of soft tissue and for in-situ non-invasive assessment and monitoring of ACS.

Our compartment syndrome model was developed on the cranial tibial and the peroneus tertius muscles of a pig's leg (postmortem). The compartment syndrome pressure values were obtained by injecting blood from the bone through the muscle.

To enable ACS assessment by a hand-held indentation device we combined three main components: a load cell, a linear actuator and a 3-axis accelerometer. Dynamic tests were performed at a frequency of 0.5 Hz and by applying an amplitude of 0.5 mm.

Another method used to observe the differences in the mechanical properties inside the leg was a 3D Digital Image Correlation (3D-DIC). Videos were taken from two different positions of the pig's leg at different pressure values: 0 mmHg, 15 mmHg and 40 mmHg. Two strains along the x axis (Exx) and y axis (Eyy) were measured.

Between the two pressure cases (15 mmHg and 40 mmHg) a clear deformation of the model is visible. In fact, the bigger the pressure, the more visible the increase in strain is.

In our animal model, local muscle pressures reached values higher than 40 mmHg, which correlate with observed human physiology in ACS. In our presentation we will share our dynamic indentation results on this model to demonstrate the sensitivity of our measurement techniques.

Compartment syndrome is recognised as needing improved clinical management tools. Our approach provides both a model that reflects physiological behaviour of ACS, and a method for in-situ non-invasive assessment and monitoring.

Introduction Damage Control orthopaedic techniques have been proposed in the seriously injured with primary external fixation of long bone fractures, reducing the ‘second hit’ of surgery. We have developed a large animal (ovine) model for the study of major trauma.

Aim To clarify the sequence of pulmonary and systemic physiological responses over a 24-hour period following injury, comparing the effects of primary external femoral fixation to intramedullary stabilisation to better quantify the ‘second hit’ of these surgical techniques.

Methods Under terminal anaesthesia bilateral femoral diaphyseal fractures were produced using a mechanical pneumatic actuator (ram). Hypovolaemic shock was maintained for 4 hours before fluid resuscitation and surgical stabilisation.

24 sheep were randomised into 4 groups and monitored for 24 hours following injury:

Group 1 – Control Group (effects of general anaesthesia only)

Group 2 – Control Group for Trauma (injury but no long bone stabilisation)

Group 3 – Damage control group (Injury and external fixation)

Group 4 – Early total care (Injury and reamed intra-medullary stabilisation)

Outcome measures: Embolic load (Mayo score) using transoesophageal echocardiography; serum markers of coagulation (prothrombin time, activated partial thromboplastin time and fibrinogen levels) and inflammation (interleukin 6). Bronchoalveolar lavage to assess total cell count and cell differential to quantify the proportion of neutrophils present.

Results A sustained embolic shower was detected with each femoral fracture (mean Mayo score of 5 and 5.5 respectively). Intramedullary reaming and nailing produced further embolic events with a mean score of 2.5 and 1.5 respectively. Mean prothrombin time increased from a pre-fracture mean of 12 in each group to 18.8 (group 1) 20.7 (group 2); 24.8 (group 3); 31.1 (group 4). Alveolar lavage samples taken at 0, 4 and 24 hours following injury indicated a progressive neutrophilia developing in each group with a count pre-fracture of 4.3 increasing to 55.75 (group 1); 40 (group2); 49 (group3) and 31.7 (group 4) by 24 hours following injury.

Discussion The effects of damage control techniques in this model appear to be a reduced stimulation of the extrinsic coagulation system. An additional embolic hit was detected secondary to intramedullary reaming and nail insertion. Localised lung inflammation seems to develop in all groups with no significant differences seen due to treatment.