The management of radial nerve palsy associated with fractures of the shaft of the humerus has been disputed for several decades. This study has systematically reviewed the published evidence and developed an algorithm to guide management. We searched web-based databases for studies published in the past 40 years and identified further pages through manual searches of the bibliography in papers identified electronically. Of 391 papers identified initially, encompassing a total of 1045 patients with radial nerve palsy, 35 papers met all our criteria for eligibility. Meticulous extraction of the data was carried out according to a preset protocol. The overall prevalence of radial nerve palsy after fracture of the shaft of the humerus in 21 papers was 11.8% (532 palsies in 4517 fractures). Fractures of the middle and middle-distal parts of the shaft had a significantly higher association with radial nerve palsy than those in other parts. Transverse and spiral fractures were more likely to be associated with radial nerve palsy than oblique and comminuted patterns of fracture (p < 0.001). The overall rate of recovery was 88.1% (921 of 1045), with spontaneous recovery reaching 70.7% (411 of 581) in patients treated conservatively. There was no significant difference in the final results when comparing groups which were initially managed expectantly with those explored early, suggesting that the initial expectant treatment did not affect the extent of nerve recovery adversely and would avoid many unnecessary operations. A treatment algorithm for the management of radial nerve palsy associated with fracture of the shaft of the humerus is recommended by the authors.

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Many authors recommend surgery to remove retropulsed bone fragments from the canal in burst fractures to 'decompress' the spinal canal. We believe, however, that neurological damage occurs at the moment of injury when the anatomy is most distorted, and is not due to impingement in the resting positions observed afterwards. We studied 20 consecutive patients admitted to our spinal injuries unit over a two-year period with a T12 or L1 burst fracture. There was no correlation between bony or canal disruption and the degree of neurological compromise sustained but there was a significant correlation between the energy of the injury (as gauged by the Injury Severity Score) and the neurological status (p < 0.001). This suggests that neurological injury occurs at the time of trauma rather than being a result of pressure from fragments in the canal afterwards and questions the need to operate simply to remove these fragments.

Spinal burst fractures account for about 15% of spinal injuries and, because of their predominance in the younger population, there are large associated social and healthcare costs. Although several experimental studies have investigated the burst fracture process, little work has been undertaken using computational methods. The aim of this study was to develop a finite element model of the fracture process and, in combination with experimental data, gain a better understanding of the fracture event and mechanism of injury. Experimental tests were undertaken to simulate the burst fracture process in a bovine spine model. After impact, each specimen was dissected and the severity of fracture assessed. Two of the specimens tested at the highest impact rate were also dynamically filmed during the impact. A finite element model, based on CT data of an experimental specimen, was constructed and appropriate high strain rate material properties assigned to each component. Dynamic validation was undertaken by comparison with high-speed video data of an experimental impact. The model was used to determine the mechanism of fracture and the postfracture impact of the bony fragment onto the spinal cord. The dissection of the experimental specimens showed burst fractures of increasing severity with increasing impact energy. The finite element model demonstrated that a high tensile strain region was generated in the posterior of the vertebral body due to the interaction of the articular processes. The region of highest strain corresponded well with the experimental specimens. A second simulation was used to analyse the fragment projection into the spinal canal following fracture. The results showed that the posterior longitudinal ligament became stretched and at higher energies the spinal cord and the dura mater were compressed by the fragment. These structures deformed to a maximum level before forcing the fragment back towards the vertebral body. The final position of the fragment did not therefore represent the maximum dynamic canal occlusion.

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