Abstract
Introduction: During the development of an externally fixated femoral fracture model in the rat a single dose of Carpofen (Rimadyl) was administered as part of the pre-operative analgesia regime. The negative effect of a NSAID on fracture repair has been well documented.
Materials and Methods: The external fixator was designed and constructed from threaded stainless steel pins and a semi-cylindrical aluminum plate. The pins were passed through the four drill holes made in the plate and were secured by nuts above and below the plate. Forty-five female Sprague-Dawley rats, aged between twelve and eighteen weeks, were used in the model. Twenty-one animals received a single subcutaneous dose of Carpofen (4mg/kg) pre-operatively. Carpofen was then excluded from the pre-operative analgesia regime and the experiment was repeated. All animals received a dose of Buprenorphine hydrochloride (Temgesic, 0.03mg/kg) and a fluid bolus (40–80ml/ kg) both pre and post operatively and antibiotic pre-operatively. Femoral fractures were created after the animals had been anaesthetised. The right femur was then exposed and a mid femoral osteotomy was made prior to the application of the fixator. Post-operative digital x-rays were taken to confirm reduction. A minimum of four animals were assigned to a group for either biomechanical strength testing or histology. Thirty-one animals in total were sacrificed at 4, 6 or 8 weeks for biomechanical strength testing. The fractured limbs were freshly dissected and stored in saline prior to testing. Both the fractured and contralateral limbs were tested mechanically by four point bending. The maximum load to failure was recorded and stiffness was calculated from the load displacement curve obtained. The bending strength of each fractured femur was expressed as a percentage of the strength of the intact contralateral femur. Fourteen fractured limbs were fixed in formaldehyde, decalcified and paraffin embedded for histological analysis. Serial sections were cut and stained with haematoxylin, eosin and Alcin blue at 4, 6 or 8 weeks.
Results: Satisfactory reduction of the fracture was confirmed post-operatively by faxtitron x-ray imaging in all animals. Preliminary data showed that there was a significant difference in stiffness at 8 weeks between the two groups (p= 0.008). Although not a significant difference, stiffness and load to failure were lower in the NSAID group at each of the three time points.
Conclusion: This data suggests that a single pre-operative dose of a NSAID is sufficient to delay fracture repair. The clinical relevance of this finding is that frequently in acute fracture patients a single dose of NSAID is given peri-operatively as it is felt that this will have no effect on fracture repair. This practice may need to be reviewed. On qualitative histology endosteal and periosteal bridging was evident in the group that did not receive NSAID at 1 and 2 weeks. Healing within the NSAID group at 4 weeks was poor.
Correspondence should be addressed to Dr Carlos Wigderowitz, Honorary Secretary of BORS, Division of Surgery & Oncology, Section of Orthopaedic & Trauma Surgery, Ninewells Hospital & Medical School Tort Centre, Dundee, DD1 9SY.
