Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Bleeding is a leading cause of death among trauma patients. Delayed assessment of blood hemoglobin level might result in either unnecessary blood transfusion in nonindicated patients or delayed blood transfusion in critically bleeding patients. In this study, we evaluate the precision of noninvasive hemoglobin monitoring in trauma patients with low hemoglobin levels. ⋯ One hundred eighty-four time-matched samples were available for final analysis. Bland-Altman analysis showed excellent accuracy of Sp-Hb compared with Lab-Hb with mean bias of 0.12 g/dL and limits of agreement between -0.56 g/dL and 0.79 g/dL. Excellent correlation was reported between both measures with Pearson correlation coefficient of 0.872. Excellent agreement was also reported between both Delta-Sp-Hb and Delta-Lab-Hb with mean bias of -0.05 and limits of agreement from -0.62 to 0.51 CONCLUSIONS:: Sp-Hb showed accurate precision in both absolute values and trend values compared with Lab-Hb measurement in trauma patients with low hemoglobin levels.
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The small molecule pifithrin-μ reversibility inhibits the mitochondrial pathway of apoptosis. The neuronal effects of pifithrin-μ applied after cardiac arrest are unknown. We hypothesized that pifithrin-μ reduces neuronal damage in the most vulnerable brain region, the hippocampus, after cardiac arrest. ⋯ Temporarily inhibition of apoptosis with pifithrin-μ after cardiac arrest decreases the number of injured neurons in the CA1 segment of hippocampus in a cardiac arrest rat model, without clinical correlate. Further studies should elucidate the role of this neuroprotective agent in different settings and with longer cardiac arrest.
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In septic patients, both systemic inflammation and splanchnic hypoperfusion may cause enterocyte damage. Catecholamines may exert additional detrimental effects on mesenteric blood flow in these patients, and thereby contribute to this damage. Enterocyte damage itself results in impairment of gut barrier function and consequent translocation of bacteria/toxins. This may contribute to multiple organ failure and death by sustaining or amplifying the systemic inflammatory response. The aim of the study was 2-fold: to investigate which factors contribute to enterocyte damage in septic patients, and to assess whether enterocyte damage is associated with a sustained or amplified systemic inflammatory response. ⋯ In patients with septic shock, norepinephrine use is associated with more enterocyte damage. Although enterocyte damage is associated with increased 28-day mortality, it is not associated with a sustained or amplified systemic inflammatory response.
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The study investigated the effect of untreated cardiac arrest (CA), that is, "no-flow" time, on postresuscitation myocardial and neurological injury, and survival in a pig model to identify an optimal duration that adequately reflects the most frequent clinical scenario. ⋯ Longer no-flow durations caused greater postresuscitation myocardial and neurological dysfunction and reduced survival. An untreated CA of 12-13 min may be an optimal choice for a clinically relevant model.