Mortality Rate In Severe Sepsis Research Articles

Performance evaluation of MR-proadrenomedullin and other scoring systems in severe sepsis with pneumonia.

In sepsis, risk assessment is as crucial as early and accurate diagnosis. In this study, we aimed to evaluate the prognostic value of mid-regional proadrenomedullin (MR-proADM) with other scoring systems in severe sepsis and septic shock patients due to community acquired pneumonia (CAP). Patients were divided into 2 groups as severe sepsis and septic shock due to CAP (group 1, n=31) and only CAP group (group 2, n=26). Serum MR-proADM, procalcitonin (PCT), C-reactive protein (CRP), and d-dimer level were analyzed. Acute Physiological and Chronic Health Evaluation (APACHE) II score, Sequential Organ Failure Assessment (SOFA) score, and Pneumonia Severity Index (PSI) were performed for all patients. There was no difference between groups in terms of serum MR-proADM levels (P=0.780). Serum MR-proADM was not found a significant value for the prediction of death within the 4 and 8 weeks in all patients. SOFA score was the most significant to predict mortality in 4 and 8 weeks (P<0.001). The combination of SOFA score and serum MR-proADM was a strong factor to predict death in 4 weeks (specifity 86.8% and sensitivity 66.7%). The combination of MR-proADM, SOFA score, and APACHE II score was found 75.0% sensitive and 71.4% specific to predict mortality within 4 weeks in group 1. The MR-proADM does not correlate with mortality or disease severity to predict mortality. The combination of SOFA, APACHE II scores, and MR-proADM was efficient to predict prognosis and mortality rate in severe sepsis or septic shock patients.

Decreasing in-hospital mortality rate in severe sepsis and septic shock patients by implementing a sepsis bundle in University Hospital, Trnava

Decreasing in-hospital mortality rate in severe sepsis and septic shock patients by implementing a sepsis bundle in University Hospital, Trnava

A Prospective Study of Comparison of APACHE-IV & SAPS-II Scoring Systems and Calculation of Standardised Mortality Rate in Severe Sepsis and Septic Shock Patients.

Severe sepsis and septic shock are major causes of mortality in the Intensive Care Unit (ICU) Illness Scoring Systems can help in the prediction of outcome of these patients. To calculate and compare APACHE-IV and SAPS-II Scoring Systems along with calculation of Standardised Mortality Rate (SMR) in patients of severe sepsis and septic shock in the ICU. Observational-analytical prospective study. The study was conducted on 84 patients with severe sepsis and septic shock admitted to the Medical ICU of a tertiary care teaching hospital. Mean of Predicted Mortality Rate (PMR) for APACHE-IV was 37.85% and for SAPS-II, it was 72.36% which shows that APACHE-IV had under-predicted overall mortality while SAPS-II had over-predicted overall mortality of patients with severe sepsis and septic shock. Standardised Mortality Rate for APACHE-IV was 1.60 and for SAPS-II, it was 0.83. Predicted Mortality of APACHE-IV and SAPS-II Scoring Systems did not correlate with the observed mortality for patients with severe sepsis and septic shock.

Continuous Renal Replacement Therapy in Pediatric Severe Sepsis: A Propensity Score-Matched Prospective Multicenter Cohort Study in the PICU.

Continuous renal replacement therapy becomes available utilization for pediatric critically ill, but the impact of mortality rate in severe sepsis remains no consistent conclusion. The aim of the study is to assess the effect of continuous renal replacement therapy in pediatric patients with severe sepsis and the impact this therapy may have on their mortality. Propensity score-matched cohort study analyzing data prospectively collected by the PICUs over 2 years (2016-2018). Four PICUs of tertiary university children's hospital in China. The consecutive patients with severe sepsis admitted to study PICUs were enrolled from July 2016 to June 2018. The patients were divided into the continuous renal replacement therapy group and the conventional (noncontinuous renal replacement therapy) group. A total of 324 patients with severe sepsis were enrolled. The hospital mortality rate was 35.6% (64/180) in the continuous renal replacement therapy group and 47.9% (69/144) in the noncontinuous renal replacement therapy group. After propensity score adjustment, the hospital mortality rate was 21.3% (29/136) in the continuous renal replacement therapy group and 32.4% (44/136) in the noncontinuous renal replacement therapy group. In subgroup analysis, the relative risk of dying was 0.447 (95% CI, 0.208-0.961) only in patients complicated by acute respiratory distress syndrome (p = 0.037), but not in patients with shock, acute kidney injury, acute liver dysfunction, encephalopathy, and fluid overload greater than 10%. The mean duration of continuous renal replacement therapy was 45 hours (26-83 hr) with an ultrafiltration rate of 50 mL/kg/hr. The level of interleukin-6 was decreased, and the percent of natural killer cells (%) was improved in the continuous renal replacement therapy group compared with the noncontinuous renal replacement therapy group. Furthermore, continuous renal replacement therapy was an independently significant risk factor for hospital mortality in pediatric patients with severe sepsis, and the interval between continuous renal replacement therapy initiation and PICU admission was an independent risk factor for hospital mortality in patients receiving continuous renal replacement therapy. Continuous renal replacement therapy with an ultrafiltration rate of 50 mL/kg/hr decreases hospital mortality rate in pediatric severe sepsis, especially in patients with acute respiratory distress syndrome.

SAT0465 TNF-β NCO1 polymorphism in relation to postoperative sepsis outcome in joint care surgery

BackgroundPostoperative sepsis remains a challenge for joint care surgeons as it is a significant cause of morbidity and mortality. It has been postulated that genetic factors may have a role...

Positive effect of septimeb™ on mortality rate in severe sepsis: a novel non antibiotic strategy

BackgroundSeptimeb is a new herbal-derived remedy, recently approved for its potential immunomodulatory effects. Regarding the key role of immune system in the pathogenesis of severe sepsis and lack of any standard treatment for improving survival of these patients; we evaluated the effect of Septimeb -as an adjutant to standard treatment-on inflammatory biomarkers and mortality rates in patients with severe sepsis.MethodsIn this multicenter, randomized, single-blind trial, we assigned patients with severe sepsis and Acute Physiology and Chronic Health Evaluation (APACHE II) score of more than 20 to receive standard treatment of severe sepsis (control group) or standard treatment plus Septimeb. This group was treated with Septimeb for 14 days then followed up for another14 days. APACHE score, Sequential Organ Failure Assessment (SOFA) and Simplified Acute Physiology Score (SAPS) were calculated daily. Blood samples were analyzed for interleukin 2 tumor necrosis factor-α, total antioxidant power, platelet growth factor and matrix metalloproteinase 2.ResultsA total of 29 patients underwent randomization (13 in control group and 16 in Septimeb group). There was significant difference between the Septimeb and control group in the 14 days mortality rate (18.8% vs. 53.85 respectively, P=0.048). Compared to control group, Septimeb was significantly effective in improving SAPS (P= 0.029), SOFA (P=0.003) and APACHE II (P=0.008) scores. Inflammatory biomarkers didn’t change significantly between the two groups (P>0.05).ConclusionSeptimeb reduces mortality rates among patients with severe sepsis and it could be added as a safe adjutant to standard treatment of sepsis.

Temporal Trends in the Epidemiology of Severe Postoperative Sepsis after Elective Surgery

Multiple studies have used administrative datasets to examine the epidemiology of sepsis in general, but the entity of postoperative sepsis has been studied less intensively. Therefore, we undertook an analysis of the epidemiology of postoperative sepsis using the Nationwide Inpatient Sample, the largest in-patient dataset available in the United States. Elective admissions of patients aged 18 yr or older with a length of stay more than 3 days for any 1 of the 20 most common elective operative procedures were extracted from the dataset for the years 1997-2006. Postoperative sepsis was defined using the appropriate International Classification of Diseases, Ninth Revision, Clinical Modification codes; severe sepsis was defined as sepsis along with organ dysfunction. Logistic regression was used to assess the significance of temporal trends after adjusting for relevant demographic characteristics, operative procedure, and comorbid conditions. We identified 2,039,776 admissions for analysis. The rate of severe sepsis increased from 0.3% in 1997 to 0.9% in 2006. This trend persisted after adjusting for relevant covariables-the adjusted odds ratio of severe sepsis per year increase in the study period was 1.12 (95% CI, 1.11-1.13; P < 0.001). The in-hospital mortality rate for patients with severe postoperative sepsis declined from 44.4% in 1997 to 34.0% in 2006; this trend also persisted after adjustment for relevant covariables-the adjusted odds ratio per year was 0.94 (95% CI, 0.93-0.95; P < 0.001). During the 10-yr period that we studied, there was a marked increase in the rate of severe postoperative sepsis but a concomitant decrease in the in-hospital mortality rate in severe sepsis.

Protein C in murine neonatal sepsis

Neonatal sepsis is frequently associated with activation of the coagulation system. Generally, protein C levels are markedly reduced in the majority of septic patients, being associated with an increased risk of death. There is an activated protein C concentrate licensed for the treatment of severe sepsis in adults. However, the risk of severe bleeding may limit its use in neonates. Since the likelihood to induce bleeding with the zymogen form of protein C may be reduced, we therefore assessed both human and recombinant murine protein C zymogen in a murine neonatal sepsis model. In this model neonatal mice were challenged with viable group B streptococci (GBS). The impact of this septic condition on endogenous protein C levels was evaluated and the effect of treatment with either recombinant murine protein C or human plasma-derived (non-activated) protein C (Ceprotin®) investigated. During severe GBS sepsis murine endogenous protein C levels decreased over time in neonatal mice, resulting in a maximum decrease of 30% at 16 hours after GBS challenge and returned towards baseline at 30 hours. Concomitantly, there was an increase in endogenous protein C activation up to 59% at 6 hours after GBS challenge, returning to baseline levels at 16 hours. Blocking endogenous murine protein C with an anti-mouse monoclonal antibody increased the mortality rate significantly from 62% to 91%. Treatment of neonatal septic mice (n = 36) with 300 U/kg murine protein C subcutaneously 4 hours before GBS challenge decreases the mortality rate significantly in severe sepsis (LD90) to 64% (P = 0.002). Similarly, pretreatment with human plasma-derived protein C (200 U/kg) 4 hours before GBS challenge increased the survival rate significantly in severe septic mice. Human plasma derived protein C at the dose of 200 IU/kg was even effective given 18 hours after GBS challenge, leading to a decrease of the mortality rate in severe sepsis from 87.5% to 48%. Despite the species differences human protein C zymogen was activated to activated protein C and was detectable in the circulation of mice, showing a slow and low in vivo recovery, possibly due to the subcutaneous route of administration. This is the first preclinical study where a beneficial effect of a non-activated protein C could be shown in an animal model of severe neonatal sepsis.

Effect of Human Plasma-Derived Protein C and Murine Recombinant Protein C on Severe Neonatal Sepsis in Mice.

Neonatal sepsis is a leading cause of infant morbidity and mortality frequently associated with activation of the coagulation system. Reduced levels of protein C are found in the majority of patients with sepsis and are associated with an increased risk of death. Although activated protein C is indicated for the treatment of severe sepsis in adults, the risk of severe bleeding may limit its use in neonates. Because the likelihood of inducing bleeding with the zymogen form of protein C is reduced we assessed both human and murine protein C zymogen in a murine neonatal sepsis model. In this model neonatal mice were challenged with viable group B streptococci (GBS). The effect of this septic condition on endogenous protein C levels was evaluated and the effect of treatment with either recombinant murine protein C or human plasma-derived (non-activated) protein C (Ceprotin) investigated. During severe GBS sepsis murine endogenous protein C levels decreased over time in neonatal mice, resulting in a maximum decrease of −30 % at 16 hours after GBS challenge and returned towards baseline at 30 hours. Concomitantly, there was an increase in endogenous protein C activation up to 59 % at 6 hours after GBS challenge, returning to baseline levels at 16 hours. Blocking endogenous murine protein C with an anti-mouse monoclonal antibody increased the mortality rate significantly from 62 to 91 %. Treatment of neonatal septic mice (n=36) with 300 U/kg murine protein C subcutaneously 4 hours before GBS challenge decreased the mortality rate significantly in severe sepsis (LD90) to 64 % (p=0.002). Similarly pretreatment with human plasma-derived protein C (200 IU/kg) 4 hours before GBS challenge increased survival rate significantly in severe septic mice. Treatment with 200 IU/kg (Ceprotin) was even effective given 18 hours after GBS challenge, leading to a decrease in the mortality rate in severe sepsis from 87.5 to 48 %. Despite this species difference and the septic condition, human protein C zymogen was activated to activated protein C and detectable in the circulation of mice. This is the first preclinical study were a beneficial effect of a non-activated protein C could be shown in an animal model of severe neonatal sepsis.

Relation of a TNF gene polymorphism to severe sepsis in trauma patients.

To investigate the relation of the biallelic Nco1 restriction fragment length polymorphism in the first intron of the tumor necrosis factor (TNF) beta gene with the development of severe sepsis in multiply injured patients. The biallelic Nco1 polymorphism of the TNFbeta gene has been described to be associated with autoimmune diseases and with the mortality rate in severe sepsis. Therefore, the Nco1 polymorphism may be associated with the clinical finding that despite comparable risk factors, posttraumatic sepsis develops in some patients but not others. The study group consisted of 110 patients with severe blunt trauma (Injury Severity Score > or = 17). Typing of each patient for the biallelic Nco1 polymorphism was performed by analyzing restriction fragments of an Nco1-digested DNA fragment obtained using polymerase chain reaction. Genotypes were then related to the occurrence of severe posttraumatic sepsis and TNFalpha serum concentrations. Fifty-seven patients showed an uncomplicated posttraumatic recovery, and severe sepsis developed in 53 patients. The overall allele frequency (TNFB1 0.29, TNFB2 0.71) and genotype distribution (TNFB1 homozygous 7.3%, TNFB1/TNFB2 42.7%, TNFB2 homozygous 50%) were in agreement with the distribution in healthy volunteers. Genotype distribution in patients with an uncomplicated clinical course was significantly different from that in patients with severe posttraumatic sepsis. Development of severe posttraumatic sepsis was significantly increased in patients homozygous for the allele TNFB2. In patients with severe posttraumatic sepsis, TNFalpha serum concentrations were significantly higher in TNFB2-homozygous individuals compared with heterozygous and TNFB1 -homozygous individuals. The age- and injury-matched odds ratio for the homozygous TNFB2 genotype compared with the heterozygous genotype was 5.22 (p = 0.007, 95% confidence interval 1.6 to 17.9). In multiply injured patients, the Nco1 polymorphism within the TNFbeta gene is associated with the development of severe posttraumatic sepsis and with increased TNFalpha serum levels when severe sepsis has occurred. This suggests a genetic determination of the individual inflammatory response after infection or tissue damage, which significantly influences susceptibility to severe nosocomial infections.