Evaluation of a survey tool to measure safety climate in Australian hospital pharmacy staff.

BACKGROUND: Safety climate evaluation is increasingly used by hospitals as part of quality improvement initiatives. Consequently, it is necessary to have validated tools to measure changes. OBJECTIVE: To evaluate the construct validity and internal consistency of a survey tool to measure Australian hospital pharmacy patient safety climate. METHODS: A 42 item cross-sectional survey was used to evaluate the patient safety climate of 607 Australian hospital pharmacy staff. Survey responses were initially mapped to the factor structure previously identified in European community pharmacy. However, as the data did not adequately fit the community pharmacy model, participants were randomly split into two groups with exploratory factor analysis performed on the first group (n = 302) and confirmatory factor analyses performed on the second group (n = 305). RESULTS: Following exploratory factor analysis (59.3% variance explained) and confirmatory factor analysis, a 6-factor model containing 28 items was obtained with satisfactory model fit (χ2 (335) = 664.61 p < 0.001, RMSEA = 0.06, CFI = 0.93, TLI = 0.92), internal reliability (α > 0.643) and model nesting between the groups (Δχ2 (22) = 30.87, p = 0.10). Three factors (blame culture, organisational learning and working conditions) were similar to those identified in European community pharmacy and labelled identically. Three additional factors (preoccupation with improvement; comfort to question authority; and safety issues being swept under the carpet) highlight hierarchical issues present in hospital settings. CONCLUSIONS: This study has demonstrated the validity of a survey to evaluate patient safety climate of Australian hospital pharmacy staff. Importantly, this validated factor structure may be used to evaluate changes in safety climate over time.

An exploration of Australian hospital pharmacists' attitudes to patient safety.

OBJECTIVES: To explore the attitudes of Australian hospital pharmacists towards patient safety in their work settings. METHODS: A safety climate questionnaire was administered to all 2347 active members of the Society of Hospital Pharmacists of Australia in 2010. Part of the survey elicited free-text comments about patient safety, error and incident reporting. The comments were subjected to thematic analysis to determine the attitudes held by respondents in relation to patient safety and its quality management in their work settings. KEY FINDINGS: Two hundred and ten (210) of 643 survey respondents provided comments on safety and quality issues related to their work settings. The responses contained a number of dominant themes including issues of workforce and working conditions, incident reporting systems, the response when errors occur, the presence or absence of a blame culture, hospital management support for safety initiatives, openness about errors and the value of teamwork. A number of pharmacists described the development of a mature patient-safety culture - one that is open about reporting errors and active in reducing their occurrence. Others described work settings in which a culture of blame persists, stifling error reporting and ultimately compromising patient safety. CONCLUSION: Australian hospital pharmacists hold a variety of attitudes that reflect diverse workplace cultures towards patient safety, error and incident reporting. This study has provided an insight into these attitudes and the actions that are needed to improve the patient-safety culture within Australian hospital pharmacy work settings.

Thiazolidinediones inhibit airway smooth muscle release of the chemokine CXCL10: in vitro comparison with current asthma therapies.

BACKGROUND: Activated mast cells are present within airway smooth muscle (ASM) bundles in eosinophilic asthma. ASM production of the chemokine CXCL10 plays a role in their recruitment. Thus the effects of glucocorticoids (fluticasone, budesonide), long-acting ß2-agonists (salmeterol, formoterol) and thiazolidinediones (ciglitazone, rosiglitazone) on CXCL10 production by ASM cells (ASMC) from people with and without asthma were investigated in vitro. METHODS: Confluent serum-deprived cells were treated with the agents before and during cytokine stimulation for 0-24 h. CXCL10 protein/mRNA, IκB-α levels and p65 activity were measured using ELISA, RT PCR, immunoblotting and p65 activity assays respectively. Data were analysed using ANOVA followed by Fisher's post-hoc test. RESULTS: Fluticasone and/or salmeterol at 1 and 100 nM inhibited CXCL10 release induced by IL-1ß and TNF-α, but not IFNγ or all three cytokines (cytomix). The latter was also not affected by budesonide and formoterol. In asthmatic ASMC low salmeterol, but not formoterol, concentrations increased cytomix-induced CXCL10 release and at 0.01 nM enhanced NF-κB activity. Salmeterol 0.1 nM together with fluticasone 0.1 and 10 nM still increased CXCL10 release. The thiazolidinediones ciglitazone and rosiglitazone (at 25 and 100 µM) inhibited cytomix-induced CXCL10 release but these inhibitory effects were not prevented by the PPAR-g antagonist GW9662. Ciglitazone did not affect early NF-κB activity and CXCL10 mRNA production. CONCLUSIONS: Thus the thiazolidinediones inhibited asthmatic ASMC CXCL10 release under conditions when common asthma therapies were ineffective or enhanced it. They may provide an alternative strategy to reduce mast cell-ASM interactions and restore normal airway physiology in asthma.

Asthmatic airway smooth muscle CXCL10 production: mitogen-activated protein kinase JNK involvement.

CXCL10 (IP10) is involved in mast cell migration to airway smooth muscle (ASM) bundles in asthma. We aimed to investigate the role of cytokine-induced MAPK activation in CXCL10 production by ASM cells from people with and without asthma. Confluent growth-arrested ASM cells were treated with inhibitors of the MAPKs ERK, p38, and JNK and transcription factor NF-κB, or vehicle, and stimulated with IL-1ß, TNF-α, or IFN-γ, alone or combined (cytomix). CXCL10 mRNA and protein, JNK, NF-κB p65 phosphorylation, and Iκ-Bα protein degradation were assessed using real-time PCR, ELISA, and immunoblotting, respectively. Cytomix, IL-1ß, and TNF-α induced CXCL10 mRNA expression more rapidly in asthmatic than nonasthmatic ASM cells. IL-1ß and/or TNF-α combined with IFN-γ synergistically increased asthmatic ASM cell CXCL10 release. Inhibitor effects were similar in asthmatic and nonasthmatic cells, but cytomix-induced release was least affected, with only JNK and NF-κB inhibitors halving it. Notably, JNK phosphorylation was markedly less in asthmatic compared with nonasthmatic cells. However, in both, the JNK inhibitor SP600125 reduced JNK phosphorylation and CXCL10 mRNA levels but did not affect CXCL10 mRNA stability or Iκ-Bα degradation. Together, the JNK and NF-κB inhibitors completely inhibited their CXCL10 release. We concluded that, in asthmatic compared with nonasthmatic ASM cells, JNK activation was reduced and CXCL10 gene expression was more rapid following cytomix stimulation. However, in both, JNK activation did not regulate early events leading to NF-κB activation. Thus JNK and NF-κB provide independent therapeutic targets for limiting CXCL10 production and mast cell migration to the ASM in asthma.