Transferring patient data to the care of the oncoming team is the point at which the patient is most vulnerable on their journey through the healthcare system. Effective handover is vital to protect patient safety and has become increasingly more important after introduction of shift patterns for junior doctors following the implementation of the European Working Time Directive. The aim was to assess whether the introduction of a standardised proforma and traffic light system, would improve weekend handover of patients in our orthopaedic unit.

Data was collected in the form of hand written data, for 3 months, in our department. This was analysed and a standardised handover sheet and traffic light system to highlight patient priority was introduced. Following a 1 week trial, the proformas were reviewed following feedback from colleagues. A re-audit was commenced and data collected for a further 2 months.

There were 108 patients handed over on weekends during the re-audit compared to the 126 in the initial audit. The handover of patient data improved across all areas, with the most improved areas in recording the patients' diagnosis (58.4% to 94.4%) and noting the results of significant or pending investigations (61.2% to 91.7%). The traffic light system improved recording the patient's condition (8.5% to 81.5%) as well as logging the urgency or frequency of patient review (25.9% to 96.8%).

Standardised proformas improve patient data transferred at handover and the traffic light system allows improved prioritisation of patients, thus improving patient safety at weekends.

Background

Increased revision rates and early failure of Metal-on-Metal (MoM) hip replacements are often due to adverse reaction to metal debris (ARMD). ARMD describes numerous symptoms in patients such as pain, osteolysis and soft tissue damage. Cobalt is a major component of MoM joints and can initiate an immune response via activation of the innate immune receptor Toll-like receptor 4 (TLR4). This leads to increased secretion of inflammatory cytokines e.g. interleukin-8 (IL-8). This study investigates whether TLR4-specific antagonists inhibit the inflammatory response to cobalt using IL-8 gene expression and protein secretion as a marker of TLR4 activation.

Background

Adverse reactions to metal debris are implicated in the failure of metal-on-metal hip arthroplasty. The peri-implant tissues are often infiltrated by leukocytes which may cause observed immunological effects, including soft tissue necrosis and osteolysis. Cobalt ions from orthopaedic implants aberrantly activate the innate immune receptor human toll-like receptor-4 (TLR4), leading to inflammatory cytokine release including interleukin-8 (IL-8). IL-8 has been shown to increase expression of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). These factors are essential for leukocyte adhesion to endothelium, which is required for leukocyte migration into tissues. This study investigates cobalt's effect on gene and protein changes in IL-8, ICAM-1 and VCAM-1 to determine their potential role in immune cell infiltration of peri-implant tissues.

Background

Metal-on-metal (MoM) hip arthroplasty has been associated with adverse reactions including pseudotumours, and osteolysis. Tissues surrounding failed MoM hip implants are often infiltrated by inflammatory cells such as monocytes and neutrophils. The mechanisms by which these cells are recruited to the tissues remain unclear. Cobalt from MoM implants activates Toll-like receptor 4 (TLR4), an immune cell surface receptor usually responsible for recognition of bacteria and prevention of sepsis. Activation by bacteria leads to secretion of pro-inflammatory cytokines which guide other immune cells to the site of inflammation. The effect of cobalt on this response is unknown and therefore this study aims to determine the effect of cobalt-mediated TLR4 activation on the migration of inflammatory cells.

Summary

Metal-on-metal hip replacements have been associated with adverse reactions including inflammatory pseudotumours and soft tissue necrosis. We have shown that cobalt can directly activate toll-like receptor 4, an immune receptor causing pro-inflammatory interleukin-8 secretion. This may contribute to adverse reaction development.