Explore the vast range of titles available.

Hydroxyethyl starch (HES) [corrected] is widely used for fluid resuscitation in intensive care units (ICUs), but its safety and efficacy have not been established in patients with severe sepsis. In this multicenter, parallel-group, blinded trial, we randomly assigned patients with severe sepsis to fluid resuscitation in the ICU with either 6% HES 130/0.42 (Tetraspan) or Ringer's acetate at a dose of up to 33 ml per kilogram of ideal body weight per day. The primary outcome measure was either death or end-stage kidney failure (dependence on dialysis) at 90 days after randomization. Of the 804 patients who underwent randomization, 798 were included in the modified intention-to-treat population. The two intervention groups had similar baseline characteristics. At 90 days after randomization, 201 of 398 patients (51%) assigned to HES 130/0.42 had died, as compared with 172 of 400 patients (43%) assigned to Ringer's acetate (relative risk, 1.17; 95% confidence interval [CI], 1.01 to 1.36; P=0.03); 1 patient in each group had end-stage kidney failure. In the 90-day period, 87 patients (22%) assigned to HES 130/0.42 were treated with renal-replacement therapy versus 65 patients (16%) assigned to Ringer's acetate (relative risk, 1.35; 95% CI, 1.01 to 1.80; P=0.04), and 38 patients (10%) and 25 patients (6%), respectively, had severe bleeding (relative risk, 1.52; 95% CI, 0.94 to 2.48; P=0.09). The results were supported by multivariate analyses, with adjustment for known risk factors for death or acute kidney injury at baseline. Patients with severe sepsis assigned to fluid resuscitation with HES 130/0.42 had an increased risk of death at day 90 and were more likely to require renal-replacement therapy, as compared with those receiving Ringer's acetate. (Funded by the Danish Research Council and others; 6S ClinicalTrials.gov number, NCT00962156.).

Background Hospitals worldwide have implemented Rapid Response Systems (RRS) to facilitate early recognition and prompt response by trained personnel to deteriorating patients. A key concept of this system is that it should prevent ‘events of omission’, including failure to monitor patients’ vital signs, delayed detection, and treatment of deterioration and delayed transfer to an intensive care unit. Time matters when a patient deteriorates, and several in-hospital challenges may prevent the RRS from functioning adequately. Therefore, we must understand and address barriers for timely and adequate responses in cases of patient deterioration. Thus, this study aimed to investigate whether implementing (2012) and developing (2016) an RRS was associated with an overall temporal improvement and to identify needs for further improvement by studying; patient monitoring, omission event occurrences, documentation of limitation of medical treatment, unexpected death, and in-hospital- and 30-day mortality rates. Methods We performed an interprofessional mortality review to study the trajectory of the last hospital stay of patients dying in the study wards in three time periods (P1, P2, P3) from 2010 to 2019. We used non-parametric tests to test for differences between the periods. We also studied overall temporal trends in in-hospital- and 30-day mortality rates. Results Fewer patients experienced omission events (P1: 40%, P2: 20%, P3: 11%, P = 0.01). The number of documented complete vital sign sets, median (Q1,Q3) P1: 0 (0,0), P2: 2 (1,2), P3: 4 (3,5), P = 0.01) and intensive care consultations in the wards ( P1: 12%, P2: 30%, P3: 33%, P = 0.007) increased. Limitations of medical treatment were documented earlier (median days from admission were P1: 8, P2: 8, P3: 3, P = 0.01). In-hospital and 30-day mortality rates decreased during this decade (rate ratios 0.95 (95% CI: 0.92–0.98) and 0.97 (95% CI: 0.95–0.99)). Conclusion The RRS implementation and development during the last decade was associated with reduced omission events, earlier documentation of limitation of medical treatments, and a temporal reduction in the in-hospital- and 30-day mortality rates in the study wards. The mortality review is a suitable method to evaluate an RRS and provide a foundation for further improvement. Trial registration Retrospectively registered.

Introduction Short term hypothermia has been suggested to have cardio protective properties in acute myocardial infarction (AMI) by reducing infarct size as assessed by troponins. There are limited data on the kinetics of these biomarkers in comatose out-of-hospital cardiac arrest (OHCA) patients, with and without AMI, undergoing targeted temperature management (TTM) in the ICU. Purpose The aim of this post hoc analyses was to evaluate and compare the kinetics of two high-sensitivity cardiac troponins in OHCA survivors, with and without acute myocardial infarction (AMI), during TTM of different durations [24 h (standard) vs. 48 h (prolonged)]. Methods In a sub-cohort (n = 114) of the international, multicentre, randomized controlled study “TTH48” we measured high-sensitive troponin T ( hs-cTnT), high-sensitive troponin I ( hs-cTnI) and CK-MB at the following time points: Arrival, 24 h, 48 h and 72 h from reaching the target temperature range of 33 ± 1 °C. All patients diagnosed with an AMI at the immediate coronary angiogram (CAG)—18 in the 24-h group and 25 in the 48-h group—underwent PCI with stent implantation. There were no stent thromboses. Results Both the hs-cTnT and hs-cTnI changes over time were highly influenced by the cause of OHCA (AMI vs. non-AMI). In contrast to non-AMI patients, both troponins remained elevated at 72 h in AMI patients. There was no difference between the two time-differentiated TTM groups in the kinetics for the two troponins. Conclusion In comatose OHCA survivors with an aetiology of AMI levels of both hs-cTnI and hs-cTnT remained elevated for 72 h, which is in contrast to the well-described kinetic profile of troponins in normotherm AMI patients. There was no difference in kinetic profile between the two high sensitive assays. Different duration of TTM did not influence the kinetics of the troponins. Trial registration : Clinicaltrials.gov Identifier: NCT01689077, 20/09/2012.

In this study, patients with severe sepsis were assigned to fluid resuscitation with starch (HES 130/0.4) or Ringer's acetate. The starch group had an increased risk of death at day 90 and increased use of renal-replacement therapy, as compared with the Ringer's acetate group. Intravenous fluids are the mainstay of treatment for patients with hypovolemia due to severe sepsis. Colloid solutions are used to obtain rapid and lasting circulatory stabilization, but there are limited data to support this practice. 1 The Surviving Sepsis Campaign guidelines recommend the use of either colloids or crystalloids, 2 but high-molecular-weight hydroxyethyl starch (HES) may cause acute kidney failure in patients with severe sepsis, as observed in two randomized trials. 3 , 4 Those trials had substantial limitations, and participants received HES solutions with a molecular weight of 200 kD and a substitution ratio (the number of hydroxyethyl groups per glucose molecule) of . . .

Clavicle fractures are common, and there has been a recent increase in surgical fixation of displaced fractures. General anesthesia is traditionally preferred for these operations because regional anesthesia can be challenging. This is partly due to a complex nerve innervation in this region, which makes the correct choice of nerve block difficult. The objective of this study was to evaluate the efficacy of a combined interscalene brachial plexus block and superficial cervical plexus peripheral nerve block as anesthesia for clavicle surgical procedures. Ten midshaft clavicle fractures were surgically repaired using a combination of an ultrasound-guided interscalene brachial plexus block and a superficial cervical plexus block as the primary anesthetic. All patients underwent surgery successfully using regional anesthesia with light sedation, without the need for rescue opioids or rescue local anesthesia. No adverse events were recorded. This case series describes a successful peripheral nerve block combination that can be used for clavicle surgery.

Purpose To compare two protocols for sedation and analgesia during therapeutic hypothermia: midazolam and fentanyl versus propofol and remifentanil. The primary outcome was the time from discontinuation of infusions to extubation or decision not to extubate (offset time). Secondary outcomes were blood pressure, heart rate, use of vasopressors and inotropic drugs, pneumonia and neurological outcome. Methods This was an open, randomised, controlled trial on 59 patients treated with therapeutic hypothermia (33–34 °C for 24 h) after cardiac arrest in two Norwegian university hospitals between April 2008 and May 2009. The intervention was random allocation to sedation and analgesia with propofol/remifentanil or midazolam/fentanyl. Results Twenty-nine patients received propofol and remifentanil, and 30 midazolam and fentanyl. Baseline characteristics were similar. Sedation and analgesia were stopped in 35 patients, and extubation was performed in 17 of these. Sedation had to be continued for 24 patients. Time to offset was significantly lower in patients given propofol and remifentanil [mean (95 % confidence intervals) 13.2 (2.3–24) vs. 36.8 (28.5–45.1) h, respectively, p  < 0.001]. Patients given propofol and remifentanil needed norepinephrine infusions twice as often (23 vs. 12 patients, p  = 0.003). Incidence of pneumonia and 3-month neurological outcome were similar in the two groups. Conclusions Time to offset was significantly shorter in patients treated with propofol and remifentanil. However, the clinical course in 40 % of patients prevented discontinuation of sedation and potential benefits from a faster recovery. The propofol and remifentanil group required norepinephrine twice as often, but both protocols were tolerated in most patients.

In 2013, a large scale (70 hectare) kelp forest restoration experiment was conducted in a sea urchin barren that had been stable for 45 years. We used 200 tons of quicklime to eradicate the sea urchin population. Kelp recovered within a year in the lime-treated sites. Quickliming did not significantly affect the abundance of non-target species. Mobile kelp fauna colonized the restored kelps, but at a slower rate than kelp and other macroalgae, probably due to slower dispersal abilities. The monitoring period (2012–2021) encompassed the expansion of invasive red king crabs, which emerged as a novel predator of sea urchins. This led to a gradual decline in sea urchin populations and facilitated kelp recovery also in the control sites. This delayed recovery does not invalid the conclusions of the short-term efficiency of the quicklime treatment, but it makes it difficult to conclude about the long-term effects. The study shows that quickliming can initiate kelp recovery within large urchin barrens. We postulate that the recovery of kelps outside the limed areas was due to crab predation, and that successful kelp restoration in areas with recruitment of sea urchins depends on a persistent top-down control of the urchins.

In 2013, a large scale (70 hectare) kelp forest restoration experiment was conducted in a sea urchin barren that had been stable for 45 years. We used 200 tons of quicklime to eradicate the sea urchin population. Kelp recovered within a year in the lime-treated sites. Quickliming did not significantly affect the abundance of non-target species. Mobile kelp fauna colonized the restored kelps, but at a slower rate than kelp and other macroalgae, probably due to slower dispersal abilities. The monitoring period (2012–2021) encompassed the expansion of invasive red king crabs, which emerged as a novel predator of sea urchins. This led to a gradual decline in sea urchin populations and facilitated kelp recovery also in the control sites. This delayed recovery does not invalid the conclusions of the short-term efficiency of the quicklime treatment, but it makes it difficult to conclude about the long-term effects. The study shows that quickliming can initiate kelp recovery within large urchin barrens. We postulate that the recovery of kelps outside the limed areas was due to crab predation, and that successful kelp restoration in areas with recruitment of sea urchins depends on a persistent top-down control of the urchins.

Insomnia is a common disorder linked with adverse long-term medical and psychiatric outcomes. The underlying pathophysiological processes and causal relationships of insomnia with disease are poorly understood. Here we identified 57 loci for self-reported insomnia symptoms in the UK Biobank (n = 453,379) and confirmed their effects on self-reported insomnia symptoms in the HUNT Study (n = 14,923 cases and 47,610 controls), physician-diagnosed insomnia in the Partners Biobank (n = 2,217 cases and 14,240 controls), and accelerometer-derived measures of sleep efficiency and sleep duration in the UK Biobank (n = 83,726). Our results suggest enrichment of genes involved in ubiquitin-mediated proteolysis and of genes expressed in multiple brain regions, skeletal muscle, and adrenal glands. Evidence of shared genetic factors was found between frequent insomnia symptoms and restless legs syndrome, aging, and cardiometabolic, behavioral, psychiatric, and reproductive traits. Evidence was found for a possible causal link between insomnia symptoms and coronary artery disease, depressive symptoms, and subjective well-being. Genome-wide association analyses identify 57 loci associated with insomnia symptoms and provide evidence of shared genetic architecture between insomnia and cardiometabolic, behavioral, psychiatric and reproductive traits.

Excessive daytime sleepiness (EDS) affects 10–20% of the population and is associated with substantial functional deficits. Here, we identify 42 loci for self-reported daytime sleepiness in GWAS of 452,071 individuals from the UK Biobank, with enrichment for genes expressed in brain tissues and in neuronal transmission pathways. We confirm the aggregate effect of a genetic risk score of 42 SNPs on daytime sleepiness in independent Scandinavian cohorts and on other sleep disorders (restless legs syndrome, insomnia) and sleep traits (duration, chronotype, accelerometer-derived sleep efficiency and daytime naps or inactivity). However, individual daytime sleepiness signals vary in their associations with objective short vs long sleep, and with markers of sleep continuity. The 42 sleepiness variants primarily cluster into two predominant composite biological subtypes - sleep propensity and sleep fragmentation. Shared genetic links are also seen with obesity, coronary heart disease, psychiatric diseases, cognitive traits and reproductive ageing. A main symptom of chronic insufficient sleep is excessive daytime sleepiness. Here, Wang et al. report 42 genome-wide significant loci for self-reported daytime sleepiness in 452,071 individuals from the UK Biobank that cluster into two biological subtypes of either sleep propensity or sleep fragmentation.