[Simulation as strategy for risk minimizing in anesthesia].
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Biomedical subjects
Publications and source records attributed to J Zieger.
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INTRODUCTION: Patient safety is determined by the performance safety of the medical team. Errors in medicine are amongst the leading causes of death of hospitalized patients. These numbers call for action. Backgrounds, methods and new forms of training are introduced in this article. METHOD: Concepts from safety research are transformed to the field of emergency medical treatment. Strategies from realistic patient simulator training sessions and innovative training concepts are discussed. RESULTS: The reasons for the high numbers of errors in medicine are not due to a lack of medical knowledge, but due to human factors and organisational circumstances. A first step towards an improved patient safety is to accept this. We always need to be prepared that errors will occur. A next step would be to separate "error" from guilt (culture of blame) allowing for a real analysis of accidents and establishment of meaningful incident reporting systems. Concepts with a good success record from aviation like "crew resource management" (CRM) training have been adapted my medicine and are ready to use. These concepts require theoretical education as well as practical training. Innovative team training sessions using realistic patient simulator systems with video taping (for self reflexion) and interactive debriefing following the sessions are very promising. CONCLUSION: As the need to reduce error rates in medicine is very high and the reasons, methods and training concepts are known, we are urged to implement these new training concepts widely and consequently. To err is human - not to counteract it is not.
Recently we observed that in human embryos and fetuses with a variety of malformations, not only malformed tissues, but also several non-malformed tissues displayed alterations in the glycosylation pattern. It was the aim of this work to investigate this more or less inexplicable phenomenon under experimental conditions. To this end, we studied a well known mouse model, the mouse mutant undulated, which has an exactly defined genetic defect (substitution in the pax-1 gene) leading to a localized malformation in the vertebral column. The glycosylation pattern was studied using lectin histochemistry. Distribution of binding sites for the lectins RCA I, Con A, SNA, SBA, PNA, LTA and WGA was studied during the organogenesis stages (i.e., days 11-18). It was striking that in mutants, changes in the glycosylation pattern were found not only in the malformed organ (i.e., vertebral anlage), but also in other embryonic tissues, which showed normal morphology. This suggests that the altered glycosylation seems to be a part of genetically determined phenomena throughout the entire organism. Our results show that a defect in a gene with a very restricted expression can cause universal changes in the glycosylation pattern during development.