Der Anaesthesist
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In 2003 an article on the future of prehospital emergency medicine in Germany was published in the journal Der Anaesthesist. Emergency medicine in Germany, which at that time was almost exclusively defined as prehospital emergency rescue, has evolved and now in-hospital domains have increasingly moved into the focus. At that time, the primary goal was to connect prehospital management with a smooth transition to hospital admission and further care in the hospital and to further optimize the rescue chain from the actual emergency through to causative treatment. ⋯ Which aspects could be developed further and become firmly established, what is still open and which questions in preclinical and clinical emergency treatment of the population will occupy us in the coming 15 years? With a critical eye to the past, the present contribution aims to capture the essential and new topics and open questions and provide a fresh perspective for the future of emergency medicine. Regulation at the state level or even lower levels of government often stand in contrast to more sweeping and economically effective approaches at the federal level. Prehospital emergency medicine in Germany is on the whole well-positioned with respect to facilities and personnel; however, as far as the economic situation and the utilization of available systems are concerned, there is still substantial room for improvement.
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Sepsis is commonly associated with loss of microvascular endothelial barrier function (capillary leak) and dysfunctional microcirculation, which both promote organ failure. The development of a distinct therapy of impaired endothelial barrier function and disturbed microcirculation is highly relevant because both of these phenomena constitute crucial processes which critically influence the prognosis of patients. ⋯ Furthermore, promising data in animal models show that therapeutic modulation of endothelial barrier function and microcirculation can be achieved by stabilizing endothelial cAMP (cyclic adenosine monophosphate) levels followed by activation of Rho-GTPase Rac1, e. g. by phosphodiesterase 4 inhibitors. This review summarizes and discusses recent findings of cellular mechanisms and in vivo trials.