BackgroundDespite the central role of nurses in intensive care, a relationship between intensive care nurse workload/staffing ratios and survival has not been clearly established. We determined whether there is a threshold workload/staffing ratio above which the probability of hospital survival is reduced and then modeled the relationship between exposure to inadequate staffing at any stage of a patient’s ICU stay and risk-adjusted hospital survival.MethodsRetrospective analysis of prospectively collected data from a cohort of adult patients admitted to two multi-disciplinary Intensive Care Units was performed. The nursing workload [measured using the Therapeutic Intervention Scoring System (TISS-76)] for all patients in the ICU during each day to average number of bedside nurses per shift on that day (workload/nurse) ratio, severity of illness (using Acute Physiology and Chronic Health Evaluation III) and hospital survival were analysed using net-benefit regression methodology and logistic regression.ResultsA total of 894 separate admissions, representing 845 patients, were analysed. Our analysis shows that there was a 95% probability that survival to hospital discharge was more likely to occur when the maximum workload-to-nurse ratio was <40 and a more than 95% chance that death was more likely to occur when the ratio was >52. Patients exposed to a high workload/nurse ratio (≥52) for ≥1 day during their ICU stay had lower risk-adjusted odds of survival to hospital discharge compared to patients never exposed to a high ratio (odds ratio 0.35, 95% CI 0.16–0.79).ConclusionsExposing critically ill patients to high workload/staffing ratios is associated with a substantial reduction in the odds of survival.Electronic supplementary materialThe online version of this article (doi:10.1186/s13613-017-0269-2) contains supplementary material, which is available to authorized users.

BackgroundSepsis coincides with altered gene expression in different tissues. Accumulating evidence has suggested that microRNAs, long non-coding RNAs, and circular RNAs are important molecules involved in the crosstalk with various pathways pertinent to innate immunity, mitochondrial functions, and apoptosis.MethodsWe searched articles indexed in PubMed (MEDLINE), EMBASE and Europe PubMed Central databases using the Medical Subject Heading (MeSH) or Title/Abstract words (“microRNA”, “long non-coding RNA”, “circular RNA”, “sepsis” and/or “septic shock”) from inception to Sep 2016. Studies investigating the role of host-derived microRNA, long non-coding RNA, and circular RNA in the pathogenesis of and as biomarkers or therapeutics in sepsis were included. Data were extracted in terms of the role of non-coding RNAs in pathogenesis, and their applicability for use as biomarkers or therapeutics in sepsis. Two independent researchers assessed the quality of studies using a modified guideline from the Systematic Review Center for Laboratory animal Experimentation (SYRCLE), a tool based on the Cochrane Collaboration Risk of Bias tool.ResultsObservational studies revealed dysregulation of non-coding RNAs in septic patients. Experimental studies confirmed their crosstalk with JNK/NF-κB and other cellular pathways pertinent to innate immunity, mitochondrial function, and apoptosis. Of the included studies, the SYRCLE scores ranged from 3 to 7 (average score of 4.55). This suggests a moderate risk of bias. Of the 10 articles investigating non-coding RNAs as biomarkers, none of them included a validation cohort. Selective reporting of sensitivity, specificity, and receiver operating curve was common.ConclusionsAlthough non-coding RNAs appear to be good candidates as biomarkers and therapeutics for sepsis, their differential expression across tissues complicated the process. Further investigation on organ-specific delivery of these regulatory molecules may be useful.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-016-1555-3) contains supplementary material, which is available to authorized users.

Autophagy is one of the innate immune defense mechanisms against microbial challenges. Previous in vitro and in vivo models of sepsis demonstrated that autophagy was activated initially in sepsis, followed by a subsequent phase of impairment. Autophagy modulation appears to be protective against multiple organ injuries in these murine sepsis models. This is achieved in part by preventing apoptosis, maintaining a balance between the productions of pro-and anti-inflammatory cytokines, and preserving mitochondrial functions. This article aims to discuss the role of autophagy in sepsis and the therapeutic potential of autophagy enhancers.

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