Objective: Shoulder instability is a common cause of morbidity amongst Professional Rugby Union players. This study explores whether the risk of shoulder dislocation is associated with innate shoulder laxity.

Methodology: We performed a pilot study where we validated techniques we used in the study and subsequently gained Ethics committee approval. The study was a controlled study, in which we visited all the Premiership Rugby Clubs in England. We assessed 169 professional rugby players (mean age 25.1 years, range 18–35) with no history of instability in either shoulder and 46 injured players with one shoulder with clinical shoulder instability symptoms (male, mean age 27.5 years, range 20–33) took part in this study. We assessed shoulder laxity by means of clinical evaluation, questionnaires and ultrasound. Anterior, posterior and inferior translation were measured in both shoulders for healthy players and the uninjured shoulder only for injured players.

Results: We found there is no significant difference between left (anterior: mean 2.92 mm, SD 1.15; posterior: mean 5.10 mm, SD 1.75; inferior: mean 3.08 mm, SD 1.00) and right (anterior: mean 3.07 mm, SD 1.14; posterior: mean 4.87 mm, SD 1.61; inferior: mean 2.91 mm, SD 0.99) shoulder in healthy players (P > 0.05). The comparison between the healthy shoulders (anterior: mean 3.00 mm, SD 1.15; posterior: mean 4.99 mm, SD 1.68; inferior: mean 3.00 mm, SD 1.00) from healthy players and the normal uninjured shoulder (anterior: mean 4.16 mm, SD 1.70; posterior: mean 6.16 mm, SD 3.04; inferior: mean 3.42 mm, SD 1.18) from injured players identified that players with unstable shoulders have a significantly higher shoulder translation in their normal shoulder than healthy players (P < 0.05).

Conclusion: This is the first study looking at laxity and the risk of shoulder dislocations in sportsmen involved in a high contact sport. These results support the hypothesis that rugby players with “lax” shoulders are more likely to sustain a dislocation or subluxation injury to one of these lax shoulders in their sport. We believe pre-season screening and targeted training may play a role in identifying those at risk and may decrease the incidence of dislocations.

Deep prosthetic infections are a significant cause of failure after arthroplastic surgery. Superficial wound infections are a risk factor for deep infections. We aimed to quantify the risk of deep infection after superficial wound infections, and analyse the microbiology of organisms grown.

We defused Superficial Infection according to the definition used by the Centre for Disease Control, and Deep Infection according to the Swedish Hip Register. We retrospectively analysed the results of 6782 THR and TKRs performed consecutively from 1988–1998. We analysed patient records, radiology and microbiological data. The latter collected prospectively by our infection control team.

We identified 81 (1. 2%) superficial wound infections, however we had to exclude 3 due to poor follow-up. Of the 78 patients studied, mean age was 71 (23–89), 50 were female, 28 male, 41 THR, 37 TKR and follow-up was a mean 49 months (12–130). The majority (81%) of organisms grown in the superficial wound infections were gram positive Staphylococci. These organisms were most frequently sensitive to Erythromycin or Flucloxacillin. All the superficial infections were treated with antibiotics, 66% settled with less than 6 weeks therapy. Deep prosthetic infections occurred in 10% of superficial infections in both THR and TKR. In 80% of cases the organism in the superficial infection caused the deep infection. Wound dehiscence, haematoma, post-op pyrexia and patient risk factors had no affect on onset of deep infection. However patients who had a wound discharge with positive microbiology and those patients in whom there was clinical doubt about the diagnosis of deep infection and thus had antibiotic therapy for more than six weeks had increased risk of deep sepsis.