Introduction. The highest incidence of recurrent shoulder instability is in young patients, surgical repair can reduce recurrent instability and improve shoulder function. This has led to an increasing rate of stabilisation and use of MRI to identify associated injuries in first time dislocations. MRA has the benefit of distending the joint and is becoming increasingly used. The aim of this study is to establish the sensitivity and specificity of MRA in the investigation of patients with traumatic anterior shoulder dislocations. Methods. A retrospective analysis of patients undergoing both magnetic resonance arthrography and arthroscopy after a traumatic anterior shoulder dislocation between January 2011 and 2014. Images were interpreted by eight musculoskeletal radiologists and arthroscopic findings were obtained from surgical notes and used as a reference. The sensitivity, specificity and positive predictive value for the different injuries were calculated. Results. 60 patients were reviewed; 88% were male, mean age was 28 years (range 18 to 50) and 27% were primary dislocations. The overall sensitivity and specificity of MRA to all associated injuries was 0.9 (CI 0.83–0.95) and 0.94 (CI 0.9–0.96) retrospectively. The lowest sensitivity was seen in osseous Bankart 0.8 (CI 0.44–0.96) and SLAP lesions 0.5 (CI 0.14–0.86). Conclusion. MRA has a high sensitivity when used to identify associated injuries in shoulder dislocation although in 8 patients (13%) arthroscopy identified an additional injury. The overall agreement between MRA and arthroscopic findings was good but identification of GHL and rotator cuff injuries was poor. Level of Evidence. IV. Conflict of Interests. The authors confirm that they have no relevant financial disclosures or conflicts of interest. Ethical approval was not sought as this was a systematic review

We have studied the effects of bupivacaine on human and bovine articular chondrocytes in vitro. Time-lapse confocal microscopy of human articular chondrocytes showed > 95% cellular death after exposure to 0.5% bupivacaine for 30 minutes. Human and bovine chondrocytes exposed to 0.25% bupivacaine had a time-dependent reduction in viability, with longer exposure times resulting in higher cytotoxicity. Cellular death continued even after removal of 0.25% bupivacaine. After exposure to 0.25% bupivacaine for 15 minutes, flow cytometry showed bovine chondrocyte viability to be 41% of saline control after seven days. After exposure to 0.125% bupivacaine for up to 60 minutes, the viability of both bovine and human chondrocytes was similar to that of control groups.

These data show that prolonged exposure 0.5% and 0.25% bupivacaine solutions are potentially chondrotoxic.