Continuing professional development (CPD) refers
to the ongoing participation in activities that keep a doctor up
to date and fit to practise once they have completed formal training.
It is something that most will do naturally to serve their patients
and to enable them to run a safe and profitable practice. Increasingly,
regulators are formalising the requirements for evidence of CPD,
often as part of a process of revalidation or relicensing. This paper reviews how orthopaedic journals can be used as part
of the process of continuing professional development. Cite this article:
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.
Surgical decompression of the spinal canal is presently accepted worldwide as the method of treatment for thoracolumbar burst fractures with neurological deficit in the belief that neurological recovery may be produced or enhanced. Our clinical and laboratory experience, however, indicates that the paralysis occurs at the moment of injury and is not related to the position of the fragments of the fracture on subsequent imaging. Since the preoperative geometry of the fracture may be of no relevance, our hypothesis, backed by more than two decades of operative experience, is that alteration of the canal by ‘surgical clearance’ does not affect the neurological outcome. We have reviewed the existing world literature in an attempt to find evidence-based justification for the variety of surgical procedures used in the management of these fractures. We retrieved 275 publications on the management of burst fractures of which 60 met minimal inclusion criteria and were analysed more closely. Only three papers were prospective studies; the remainder were retrospective descriptive analyses. None of the 60 articles included control groups. The design of nine studies was sufficiently similar to allow pooling of their results, which failed to establish a significant advantage of surgical over non-surgical treatment as regards neurological improvement. Significant complications were reported in 75% of papers, including neurological deterioration. Surgical treatment for burst fracture in the belief that neurological improvement can be achieved is not justified, although surgery may still occasionally be indicated for structural reasons. This information should not be withheld from the patients.
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.
