Critical care : the official journal of the Critical Care Forum
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Biguanide poisoning is associated with lactic acidosis. The exact mechanism of biguanide-induced lactic acidosis is not well understood. In the previous issue of Critical Care, Protti and colleagues demonstrated that biguanide-induced lactic acidosis may be due in part to a reversible inhibition of mitochondrial respiration. Thus, in the absence of an antidote, increased drug elimination through dialysis is logical.
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Sepsis in critically ill patients is almost associated with bad prognosis and its early detection may improve the prognosis. However, it is difficult to monitor the immunological state of these patients depending on the traditional markers of infection or inflammatory mediators. Accelerated lymphocyte death may reflect good idea about the prognosis especially when combined with 20S proteasome determinations, a recently discovered marker for muscle degradation in patients with sepsis. The hypothesis of the present study is to evaluate the role of serum 20S proteasome at early diagnosis of sepsis and its correlation with lymphocyte apoptosis to predict prognosis and consequently the early interference in critically ill patients suffering from a broad range of diseases in the intensive care unit. ⋯ The correlation of median values of 20S proteasome and the percentage of apoptotic lymphocyte median values could be a good indicator of patient prognosis and survival in critically ill patients.
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Our objective was to describe self-sufficiency and quality of life one year after intensive care unit (ICU) discharge of patients aged 80 years or over. ⋯ Among patients aged 80 or over who were selected at ICU admission, 80% were self-sufficient for activities of daily living one year after ICU discharge, 31% were alive, with no change in self-sufficiency and with similar quality of life to that of the general population matched on age and sex. However, these results must be interpreted cautiously due to the small sample of survivors.
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Ischemia and reperfusion after cardiopulmonary resuscitation (CPR) induce endothelial activation and systemic inflammatory response, resulting in post-resuscitation disease. In this study we analyzed direct markers of endothelial injury, circulating endothelial cells (CECs) and endothelial microparticles (EMPs), and endothelial progenitor cells (EPCs) as a marker of endothelial repair in patients after CPR. ⋯ In the present study we provide evidence for a severe endothelial damage after successful CPR. Our results point to an ongoing process of endothelial injury, paralleled by a subsequent endothelial regeneration 24 hours after resuscitation.
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Sedation protocols are needed for neurointensive patients. The aim of this pilot study was to describe sedation practice at a neurointensive care unit and to assess the feasibility and efficacy of a new sedation protocol. The primary outcomes were a shift from sedation-based to analgesia-based sedation and improved pain management. The secondary outcomes were a reduction in unplanned extubations and duration of sedation. ⋯ Our pilot study showed feasibility and partial efficacy of our protocol. Some neurointensive patients might not benefit from protocolized practice. We recommend an interdisciplinary effort to target patients requiring less sedation, as issues of oversedation and inadequate pain management still need more attention.