Sleep quality of patients in intensive care unit (ICU) has been recently recognized as an important aspect of the intensive care. Dexmedetomidine is one of the most recently introduced for sedation in the ICU. This study was designed to evaluate the effect of dexmedetomidine on sleep quality of patients without mechanical ventilation in ICU.The patients who were included in this study were divided into two groups. In the sedation group, dexmedetomidine was given by a continuous infusion targeting a sedation level –1 to –2 on the score of RASS (Richmond Agitation-Sedation Scale). In the no sedation group, the patients slept by themselves. No other sedatives were given. Bispectral Index (BIS) was performed on these hemodynamically stable critically ill patients for 12 consecutive hours. Sleep time and sleep depth were recorded.Twenty patients were studied. Compared to no sedation group, sleep efficiency and sleep time of patients in the sedation group was significantly higher during the night. Moreover, there was no significantly difference between the changes of blood pressure, heart rate, and respiratory rate.Dexmedetomidine is a clinically effective and safe sedative for the highly selected critically ill patients without endotracheal tube and mechanical ventilation in the ICU to increases total sleep time and improve sleep efficiency.

Purpose Sepsis-associated coagulopathy (SAC) contributes to the development of multiple organ failure (MOF) and increasing mortality. The present study was conducted to investigate whether coagulative biomarkers on admission to the intensive care unit (ICU) can predict acute kidney injury (AKI) and mortality in patients with septic shock caused by intra-abdominal infection (IAI). Patients and methods An observational retrospective study was conducted in the surgical ICU. We studied patients who met the criteria of septic shock (Sepsis-3) caused by IAI between January 1, 2013, and December 31, 2016. By adjusting for baseline characteristics, multivariate regression analyses were employed to identify independent risk factors for predicting AKI and mortality. Results Of the 138 enrolled patients, 65 patients developed AKI. The patients who developed AKI exhibited a dramatically higher Sequential Organ Failure Assessment (SOFA) score (median, 12), Acute Physiology and Chronic Health Evaluation (APACHE) II score (median, 27.5) and mortality rate. In both models, we found that activated partial thromboplastin time (APTT) (odds ratio (OR)=1.074, 95% confidence interval (CI) 1.030–1.120, p =0.001), prothrombin time (PT) (OR=1.162, 95% CI 1.037–1.302, p =0.010) and D-dimer level (OR=1.098, 95% CI 1.002–1.202, p =0.045) on admission to the ICU were significant risk factors for AKI. Moreover, Cox regression analysis showed that prolonged APTT (OR=1.065, 95% CI 1.025–1.107, p =0.001) was independently associated with high mortality. Conclusion In patients with septic shock caused by IAI, APTT, PT and D-dimer level on admission to the ICU were significantly associated with AKI. Furthermore, APTT was an independent predictor of 30-day mortality.

Ischemic stroke is a common cause of permanent disability in adults worldwide. Inflammation plays a significant role in the pathogenesis of ischemic stroke and its mechanism is complex. Both pro-inflammatory and anti-inflammatory mediators are involved in the pathogenesis of ischemic stroke, an imbalance of which leads to inflammation. Inflammatory cells from both the innate and acquired immune systems are involved in ischemic stroke-related inflammation; processes that are linked by the action of interleukin-17A (IL-17A). Although most inflammatory cells promote inflammation, T regulatory cells (Tregs) may have a protective function at the early stages of an ischemic injury, but a negative role during later stages. However, the precise mechanism of inflammation in ischemic stroke remains elusive; further understanding of it may provide new ideas for the prevention and treatment of ischemic stroke. In this review, we discuss the role of pro-inflammatory and anti-inflammatory mediators and related immune cells in the pathogenesis of ischemic stroke.

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