SIRS (systemic inflammatory response syndrome) may result from a wide variety of non-infective insults. Surgery is a recognized cause of SIRS, the onset of which can have adverse prognostic significance. Neutrophil activation is a key histopathological feature of SIRS, and neutrophil clearance through programmed cell death or apoptosis is an essential step in its resolution. Increasingly, it is recognized that ROS (reactive oxygen species), such as those generated by activated neutrophils during cardiac surgery, may have a regulatory role, influencing neutrophil lifespan and thus inflammation. In this review, we discuss the continuing importance of SIRS as a herald of inflammation and the role of neutrophil longevity in the resolution of inflammation, and we consider recent evidence for the regulation of neutrophil apoptosis by ROS.

Changes in iron homeostatic responses routinely accompany infectious or proinflammatory insults. The systemic inflammatory response syndrome (SIRS) and the development of acute lung injury (ALI) feature pronounced systemic and lung-specific alterations in iron/heme mobilization and decompartmentalization; such responses may be of pathological significance for both the onset and progression of acute inflammation. The potential for excessive iron-catalyzed oxidative stress, altered proinflammatory redox signaling, and provision of iron as a microbial growth factor represent obvious adverse aspects of altered in vivo iron handling. The release of hemoglobin during hemolytic disease or surgical procedures such as those utilizing cardiopulmonary bypass procedures further impacts on iron mobilization, turnover, and storage with associated implications. Genetic predisposition may ultimately determine the extent to which SIRS and related syndromes develop in response to such changes. The design of specific therapeutic interventions based on endogenous stratagems to limit adverse aspects of altered iron handling may prove of therapeutic benefit for the treatment of SIRS and ALI.

Both low minimum and high maximum levels of arterial carboxyhemoglobin were associated with increased intensive care mortality. Although the heme oxygenase system is protective, excessive induction may be deleterious. This suggests that there may be an optimal range for heme oxygenase-1 induction.

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ObjectiveTo assess predictive performance of universal early warning scores (EWS) in disease subgroups and clinical settings.DesignSystematic review.Data sourcesMedline, CINAHL, Embase and Cochrane database of systematic reviews from 1997 to 2019.Inclusion criteriaRandomised trials and observational studies of internal or external validation of EWS to predict deterioration (mortality, intensive care unit (ICU) transfer and cardiac arrest) in disease subgroups or clinical settings.ResultsWe identified 770 studies, of which 103 were included. Study designs and methods were inconsistent, with significant risk of bias (high: n=16 and unclear: n=64 and low risk: n=28). There were only two randomised trials. There was a high degree of heterogeneity in all subgroups and in national early warning score (I2=72%–99%). Predictive accuracy (mean area under the curve; 95% CI) was highest in medical (0.74; 0.74 to 0.75) and surgical (0.77; 0.75 to 0.80) settings and respiratory diseases (0.77; 0.75 to 0.80). Few studies evaluated EWS in specific diseases, for example, cardiology (n=1) and respiratory (n=7). Mortality and ICU transfer were most frequently studied outcomes, and cardiac arrest was least examined (n=8). Integration with electronic health records was uncommon (n=9).ConclusionMethodology and quality of validation studies of EWS are insufficient to recommend their use in all diseases and all clinical settings despite good performance of EWS in some subgroups. There is urgent need for consistency in methods and study design, following consensus guidelines for predictive risk scores. Further research should consider specific diseases and settings, using electronic health record data, prior to large-scale implementation.PROSPERO registration numberPROSPERO CRD42019143141.