The objective of this study was to assess the accuracy of blind placement of caudal epidural needles and the usefulness of the radio-contrast epidurogram. The study involves a prospective case series of 147 consecutive patients with radiological assessment of blind needle placement and epidurogram assessing the accuracy of blind needle placement in caudal epidurals. When the surgical miss rate (26%) and failure of flow of the therapeutic agents (6%) are combined, it can be deduced that up to 32% of nonradiologically guided caudal epidurals may fail to deliver the therapeutic agents to the site of pathology. There was no significant difference in the accuracy of needle placement in adequately trained and experienced middle grade surgeons when compared with consultant surgeons performing these procedures regularly. In conclusion, we recommend radiological guidance and use of epidurogram as the gold standard for the administration of caudal epidurals to increase the likelihood of successful delivery of the therapeutic agents to the site of pathology during the procedure.

Over the last 15 years, great improvements in genetic engineering and genetic manipulation strategies have led to significant advances in the understanding of the genetics governing embryological limb development. This field of science continues to develop, and the complex genetic interactions and signalling pathways are still not fully understood. In this review we will discuss the roles of the principle genes involved in the three-dimensional patterning of the developing limb and will discuss how errors in these signalling cascades correlate to congenital limb deformity in humans. This review is aimed at orthopaedic surgeons wishing to understand the principles of congenital limb deformity related to genetic signalling errors. It is by no means a comprehensive study of the molecular genetics governing the complex interactions involved in each step of limb development. There are however many syndromes involving limb deformity for which the molecular causes are unknown.

A case is reported of a post-traumatic olecranon bursitis caused by Mycobacterium kansasii following an injury sustained in a public swimming pool. It responded to surgical debridement and combined rifampicin, isoniazid, pyrazinamide and ethambutol antimicrobial therapy. A literature search was performed and a treatment regimen for this uncommon condition is suggested. Case reportA 59-year-old male with no pre-existing risk factors for tuberculous disease sustained a 2 cm laceration over his right elbow whilst at a public swimming pool. He developed an olecranon bursitis and was given a course of oral flucloxacillin and subsequently had the bursa aspirated and injected with a steroid. When the bursa ruptured he had a formal surgical excision and the specimen was sent for microbiological and histological assessment.Two weeks post-operation it was noted that the wound had not healed and had continued to ooze. Histology of the specimen showed an acute and chronic inflammatory infiltrate, focal micro-abscess and granulomas with Langerhans-type multinucleated giant cells, and an acidfast bacillus was identified on Ziehl-Neelsen stain. An atypical environmental mycobacterium was suspected, so he was started on a 6-month quadruple therapy regimen of rifampicin, isoniazid, pyrazinamide and ethambutol.Our local mycobacterial reference laboratory (Regional Centre for Tuberculosis Bacteriology, Public Health Laboratory Service, Dulwich, UK) cultured the samples on Lowenstein-Jensen medium incubated at 37 and 25 u C and assessed its photochromogenic properties. The organism was identified as Mycobacterium kansasii.When reviewed at 1 year, his elbow wound had completely healed and there was no sign of recurrence.

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