Audit of the use of antimicrobial prophylaxis in nasal surgery at a specialist Australian hospital.

BACKGROUND: In 2002-03 a retrospective audit of the use of surgical antimicrobial prophylaxis (AMP) for elective nasal surgery was undertaken at the Royal Victorian Eye and Ear Hospital (RVEEH). The RVEEH is a publicly funded teaching hospital that provides specialist eye, nose and throat medicine in Victoria, Australia. The aim of the audit was to determine the extent to which the use of antimicrobial prophylaxis in the hospital was consistent with Australian and international evidence-based guidelines and if there was a need for the hospital to develop internal guidelines for the use of AMP. METHODS: The histories of 500 consecutive patients who had undergone nasal surgery within the study period of August 2001 and July 2002 were examined. The data collected from these histories included information such as the patients' age, gender, diagnosis, surgical procedure performed, antimicrobial agents used, and the length of follow up and a range of factors shown in previous studies to increase the risk of surgical site infection. RESULTS: A total of 306 (72.86%) patients were found to have received antimicrobial agents either prior to admission, during admission or on discharge. Only 24 patients (5.71%) were administered antimicrobials immediately prior to surgery and at no other time. CONCLUSIONS: The findings of this study support the need for further research to examine the appropriateness of the use of AMP at the RVEEH and the need for internal guidelines for its use.

Heart and liver defects and reduced transforming growth factor beta2 sensitivity in transforming growth factor beta type III receptor-deficient embryos.

The type III transforming growth factor beta (TGFbeta) receptor (TbetaRIII) binds both TGFbeta and inhibin with high affinity and modulates the association of these ligands with their signaling receptors. However, the significance of TbetaRIII signaling in vivo is not known. In this study, we have sought to determine the role of TbetaRIII during development. We identified the predominant expression sites of TbetaRIII mRNA as liver and heart during midgestation and have disrupted the murine TbetaRIII gene by homologous recombination. Beginning at embryonic day 13.5, mice with mutations in TbetaRIII developed lethal proliferative defects in heart and apoptosis in liver, indicating that TbetaRIII is required during murine somatic development. To assess the effects of the absence of TbetaRIII on the function of its ligands, primary fibroblasts were generated from TbetaRIII-null and wild-type embryos. Our results indicate that TbetaRIII deficiency differentially affects the activities of TGFbeta ligands. Notably, TbetaRIII-null cells exhibited significantly reduced sensitivity to TGFbeta2 in terms of growth inhibition, reporter gene activation, and Smad2 nuclear localization, effects not observed with other ligands. These data indicate that TbetaRIII is an important modulator of TGFbeta2 function in embryonic fibroblasts and that reduced sensitivity to TGFbeta2 may underlie aspects of the TbetaRIII mutant phenotype.