Post-natal vasculogenesis, the process by which vascular committed bone marrow stem cells or endothelial precursor cells migrate, differentiate and incorporate into the nacent endothelium and thereby contribute to physiological and pathological neurovascularisation, has stimulated much interest. Its contribution to neovascularisation of tumours, wound healing and revascularisation associated with ischaemia of skeletal and cardiac muscles is well established. We evaluated the responses of endothelial precursor cells in bone marrow to musculoskeletal trauma in mice.

Bone marrow from six C57 Black 6 mice subjected to a standardised, closed fracture of the femur, was analysed for the combined expression of cell-surface markers stem cell antigen 1 (sca-1⁺) and stem cell factor receptor, CD117 (c-kit⁺) in order to identify the endothelial precursor cell population. Immunomagnetically-enriched sca-1⁺ mononuclear cell (MNC^sca-1+) populations were then cultured and examined for functional vascular endothelial differentiation. Bone marrow MNC^{sca-1+,c-kit+} counts increased almost twofold within 48 hours of the event, compared with baseline levels, before decreasing by 72 hours.

Sca-1⁺ mononuclear cell populations in culture from samples of bone marrow at 48 hours bound together Ulex Europus-1, and incorporated fluorescent 1,1′-dioctadecyl- 3,3,3,’3′-tetramethylindocarbocyanine perchlorate-labelled acetylated low-density lipoprotein intracellularily, both characteristics of mature endothelium.

Our findings suggest that a systemic provascular response of bone marrow is initiated by musculoskeletal trauma. Its therapeutic manipulation may have implications for the potential enhancement of neovascularisation and the healing of fractures.

Aims: Pharmocological modulation of skeletal muscle reperfusion injury after an ischaemic insult may improve limb salvage rates and prevent the associated systemic sequelae. Activated Protein c (APC) is an endogenous anti-coagulant with anti-inflammatory properties. The purpose of our study was to evaluate the effects of APC on skeletal muscle ischaemia reperfusion injury and to examine the direct effects of APC on neutrophil activation.

Methods: Adult male Sprague Dawley rats (n=30) were randomised into three groups: control group, I/R group treated with normal saline and I/R treated with APC. Bilateral hind-limb ischaemia was induced by rubber ban application proximal to the level of the greater trochanters for two hours. Treatment groups received either normal saline or APC prior to tourniquet release. Following twelve hours reperfusion, the tibialis anterior was dissected and muscle function assessed electrophysiologically by electrical field stimulation. The animals were then sacrificed and skeletal muscle harvested for evaluation. Skeletal muscle injury was assessed based on myeloperoxidase content, wet-to-dry ratio and histological analysis. The effect of APC on TNF-α stimulated human peripheral blood neutrophils was also examined by measuring CD 18 expression and reactive oxygen species (ROS) generation.

Results: APC significantly attenuated skeletal muscle reperfusion injury as shown by reduced myeloperoxidase content, wet-to-dry ratio and electrical properties of skeletal muscle. These findings were supported by our histological findings. Our in-vitro work demonstrated a reduction in CD 18 expression and ROS generation.

Conclusion: Activated Protein C may have a protective role in the setting of skeletal muscle ischaemia reperfusion injury and this is in part mediated by a direct inhibitory effect on neutrophil activation.

Aim: To evaluate the effect of traction on the compartment pressures during intramedullary nailing of closed tibial shaft fractures.

Materials and Methods: The study design was a randomised prospective trial. The period of the study was September 1999 to December 2000. 30 consecutive patients with Tscherne C1 fractures were randomised into two groups. 16 patients underwent intramedullary nailing of the tibia with traction and 14 patients with traction. Compartment pressures were measured before the application of traction or commencement of the procedure and at the end of the procedure. The method described by Guilli and Templeman was used to measure all the four compartments of the injured limb. The pressures were measured with a Stryker® pressure monitor. The absolute and differential compartment pressures were recorded. All patients were followed up for the duration of at least 8 months and until fracture union.

Results: The data collected was analysed using paired student t-test. There was no statistically significant difference (p> 0.05) in the preoperative mean compartment pressures for both groups when all the four compartments were measured individually. The mean postoperative measurements were higher (range 9–10 mmHg) in all four compartments in the traction group. This was statistically significant (p< 0.05). None of the pressures reached the critical level as they were more than 30 mmHg below the diastolic pressure (differential pressure).

Conclusions: These results show that traction increases compartment pressures during intramedullary nailing of tibial shaft fractures. The group considered did not have compartment syndrome possibly due to less soft tissue injury. With greater soft tissue injury and greater preoperative compartment pressures, compartment pressures can reach a critical level necessitating decompression. We conclude that intramedullary nailing without traction reduces the chances of significant increase in compartment pressures and advocate the procedure be done without traction.

Abstract: The importance of nerve root inflammation accompanying disc herniation and its contribution to symptomatology was first proposed in the 1950’s. This encouraged the widespread administration of (percutaneous) epidural steroid injections in the non-surgical treatment of acute and chronic lumbar Radicular pain. It also prompted the local application of steroid preparations directly onto the nerve root at the time of disc compression.

The literature supporting this latter practice however, is scant and equivocal. A randomised double blind prospective study was therefore carried out to evaluate the benefits of epidural steroid application at the time of lumbar disc decompression. 50 consecutive patients undergoing elective lumbar discectomy were enrolled. Patients in the study group (n=25) received 20mg of tri-amcinolone acetonide, applied directly to the decompressed nerve root. The control group (n=25) received an equal volume of saline. Intraoperative analgesia was standardised and postoperative pain was measured by a 10cm visual analog pain scale at 2, 6, 12, 25 and 72 hours. Standardised post-operative analgesic protocols were established and the amounts of consumed analgesics were determined.

Statistical analysis was performed using the Mann-Whitney test. No statistically significant difference was noted in either pain score, analgesic consumption at 24, 38 or 72 hours or length of hospital stay, between the steroid treatment or control groups. This suggests that local epidural steroid administration after lumbar disc decompression offers no therapeutic advantage over mechanical decompression alone.