Session IX - Tibia


Sunday, October 24, 1999 Session IX, Paper #68, 11:15 a.m.

Acute Compartment Syndrome: Its Effect on Bone Blood Flow and Bone Union

Margaret M. McQueen, MD; R Fleming BSc(Hons); E. Draper, Edinburgh Orthopaedic Trauma Unit, Edinburgh, Scotland

Purpose: To examine the effect of an experimentally induced acute compartment syndrome on bone blood flow and bone union.

Methods: Thirty-six New Zealand White rabbits underwent unilateral mid-diaphyseal tibial osteotomy which was stabilised with intramedullary Kirschner (K) wires. Half were subjected to an experimentally induced compartment syndrome using a balloon inflated to 90mmHg in the anterior compartment. The other half had a balloon inserted but not inflated. The balloons were deflated and removed after 24 hours. The animals were sacrificed after 24 hours, 2 weeks or 6 weeks, when tibialis anterior muscle specimens were removed for histological analysis.

The mechanical properties of the bones were measured using a torsional testing jig and the data analysed to give values for the torsional stiffness, the maximum torque and the total energy to failure. After torsional testing the experimental tibiae were reconstructed and callus and cortical area measured using an image analysis system. Both bone and muscle blood flow were assessed using radioactive microspheres. The bone was divided into proximal and distal metaphyses and proximal, middle and distal third diaphyseal segments for radioactive counting.

The values for bone blood flow and the mechanical properties were expressed as ratios of the control leg in order to minimise the variation between animals.

Statistical analyses were performed using the Wilcoxon rank sum test and the paired Wilcoxon test.

Results: The muscle histology and blood flow measurements confirmed the successful induction of muscle ischaemia and therefore an experimentally induced compartment syndrome.

Twenty-four hours after osteotomy, reductions in bone blood flow were seen in the experimental animals compared to the control animals in the whole tibial diaphysis and in the middle and distal third of the diaphysis, although these just failed to reach statistical significance. Results were similar at two weeks after osteotomy. However, at six weeks there is a statistically significant increase in blood flow in the whole diaphysis of the tibia in the control group (p < 0.05).

At six weeks there are clear differences in the mechanical strength of the tibiae in the two groups. The control group on average have regained 90% of their torsional stiffness compared to only 60% in the experimental group (p < 0.01) and 90% of their maximum torque moment compared to 50% in the experimental group(p < 0.05). Three tibiae in the experimental group failed through the osteotomy site and three partly through the osteotomy and partly through the diaphysis. None of the control group failed through the osteotomy. Two failed partly through the osteotomy and four through the distal third of the tibia with no effect on the osteotomy site.

In the experimental group the volume of callus is significantly higher than in the control group (p < 0.05) with histologically more immature callus in the experimental group.

Discussion and conclusions: This study has demonstrated a clear relationship between experimentally induced acute compartment syndrome and a delay in tibial union both mechanically and histologically. Mechanical results show a reduction in the strength of healing and histological results show an increased amount of immature callus in the experimental group. These results imply a delay in the normal evolution of the healing process.

The trend towards an increased reduction in bone blood flow in the early stages after osteotomy and acute compartment syndrome suggests a relative bone ischaemia at this time. At six weeks the control blood flow has returned to normal but a persistent hyperaemia is seen in the experimental group. This implies a delay in the normal progression of recovery of bone blood flow.

Extraosseous blood flow derived from the surrounding soft tissues is known to be crucial in the early stages after fracture as the main blood supply for the evolving callus. Muscle ischaemia has been shown in this study to cause bone ischaemia and delayed union, probably by an effect on the interosseous supply. This confirms previous clinical observations and further supports the absolute need for early recognition and prompt treatment of the acute compartment syndrome in order to avoid complications.