Multisystem Organ Failure of Sepsis Publications (5122)
Multisystem Organ Failure of Sepsis Publications
Patients underwent definitive fixation within 36 hours if one of the following three parameters were met: lactate < 4.0 mmol/L; pH ≥ 7.25; or base excess (BE) ≥ -5.5 mmol/L. If all three parameters were met, resuscitation was designated full protocol resuscitation (FPR). If less than all three parameters were met, it was designated an incomplete protocol resuscitation (IPR). Complications were assessed by an independent adjudication committee and included infection; sepsis; PE/DVT; organ failure; pneumonia, and acute respiratory distress syndrome (ARDS).
In total, 66 patients (19.7%) developed 90 complications. An historical cohort of 1441 patients had a complication rate of 22.1%. The complication rate for patients with only one EAC parameter at the point of protocol was 34.3%, which was higher than other groups (p = 0.041). Patients who had IPR did not have significantly more complications (31.8%) than those who had FPR (22.6%; p = 0.078). Regression analysis showed male gender and injury severity score to be independent predictors of complications.
This study highlights important trends in the IPR and FPR groups, suggesting that differences in resuscitation parameters may guide care in certain patients; further study is, however, required. We advocate the use of the existing protocol, while research is continued for high-risk subgroups. Cite this article: Bone Joint J 2017;99-B:122-7.
The need for better treatment strategies for STBI has led to investigations of the positive therapeutic effects of corticosteroids (CS). About 10 to 15 years ago research showed the inexpediency of CS in STBI therapy, but there were also contradictory findings showing their effectiveness. STBI is frequently followed by severe sepsis, which is not usually treated with CS. No scientific papers investigated the usage or non-usage of CS in patients with STBI followed by severe sepsis and ARDS.
The aim of the study was to investigate the influence of CS usage on treatment results in patients with STBI followed by severe sepsis and ARDS.
The study involved an analysis of the treatment results in 267 patients with STBI followed by severe sepsis and ARDS, who were treated with and without CS.
The study showed that patients' mortality decreased 1.24 times with CS use (500 mg/day of Solu-Medrol® for three days, followed by dose reduction by one-half every 3 days). Patients who took CS survived longer than patients without this treatment. The duration mechanical ventilation was shorter in patients who were treated with CS compared to the other group.
Further research into CS use is needed to improve treatment strategies for STBI followed by severe sepsis and ARDS.
Wistar rats were allocated into Sham, CLP, Sham+celecoxib, CLP+celecoxib subgroups. 2h after Sham and CLP operations, celecoxib (0.5mg/kg) or vehicle (saline; 1mL/kg) was administered orally to rats. 18h after drug administrations, MABF and responses of isolated aortic rings to phenylephrine were measured. Tissue samples were obtained for biochemical and histopathological examinations. Furthermore, survival rate was monitored throughout 96h.
Celecoxib ameliorated mesenteric hypoperfusion and partially improved aortic dysfunction induced by CLP. Survival rate was%0 at 49th h in CLP group, but in CLP+celecoxib group it was 42.8% at the end of 96h. Serum AST, ALT, LDH, BUN, Cr and inflammatory cytokine (tumor necrosis factor-alpha, interleukin-1 beta and interleukin-6) levels were increased in CLP group that were prevented by celecoxib. The decreases in liver and spleen glutathione levels and the increases in liver, lung, spleen and kidney malondialdehyde levels in CLP group were blocked by celecoxib. The histopathological protective effects of celecoxib on organ injury due to CLP were also observed.
Celecoxib has protective effects on sepsis due to its preservative effects on mesenteric perfusion, aortic function and its anti-inflammatory and antioxidative effects.
We previously reported the small-molecule modulator, inflachromene (1d), which inhibits the release of HMGBs and, thereby, reduces the production of pro-inflammatory cytokines. In this context, we intraperitoneally administered 1d to a cecal ligation and puncture (CLP)-induced mouse model of sepsis and confirmed that it successfully ameliorated sepsis pathogenesis. On the basis of a structure-activity relationship study, we discovered new candidate compounds, 2j and 2l, with improved therapeutic efficacy in vivo. Therefore, our study clearly demonstrates that the regulation of HMGB1 release using small molecules is a promising strategy for the treatment of sepsis.
Baseline characteristics, SOFA score variables, and 1-month outcome of patients were recorded and screening performance characteristics of the score were calculated using STATA 11 software.
140 patients with the mean age of 68.36 ± 18.62 years (18-95) were included (53.5% male). The most common complaints were decrease in level of consciousness (76.43%) and sepsis (60.0%), were the most frequent final diagnoses. Mean SOFA score of the patients was 7.13 ± 2.36 (minimum 2 and maximum 16). 72 (51.43%) patients died during the following 30 days and 16 (11.43%) patients were affected with multiple organ failure. Area under the ROC curve of SOFA score in predicting mortality of studied patients was 0.73 (95%CI: 0.65-0.81) (Fig. 2). Table 2 depicts screening performance characteristics of this scale in prediction of 1-month mortality in the best cut-off point of ≥7. At this cut-off point, sensitivity and specificity of SOFA in predicting 1-month mortality were 75% and 63.23%, respectively.
Findings of the present study showed that SOFA scoring system has fair accuracy in predicting 1-month mortality of critically ill patients. However, until a more reliable scoring system is developed, SOFA might be useful for narrative prediction of patient outcome considering its acceptable likelihood ratios.
We performed a systematic search of articles indexed in Pubmed, ISI Web of Knowledge, EmBase and Scopus database from inception to October 2016. Both preclinical and clinical studies investigating the role of host defense peptides in pathogenesis and as biomarkers for sepsis were included.
Of the available literatures, cathelicidin, defensin and hepcidin are amongst the best-characterized peptides. These regulate immune response, and crosstalk with pyroptosis and coagulation cascades. The applicability of these peptides as septic biomarkers has been investigated in vitro and in vivo studies. However, numerous studies were based on endotoxemia without an infection, jeopardizing interpretation of the outcomes. Cathelicidin and defensin were frequently reported in adult sepsis while hepcidin in neonatal sepsis. The expression level of these peptides is significantly associated with septic condition. Most of the studies employed a cross-sectional design, precluding the establishment of a temporal relationship between candidate peptide biomarkers and sepsis.
Innate defense peptides have been insufficiently evaluated as either diagnostic or prognostic biomarkers. In the future, evaluation of host defense peptides as septic biomarkers may employ a longitudinal design and consider a panel of multiple peptides.
It is present at high concentrations in blood and lymph and at very low concentrations in tissues due to the activity of the S1P-degrading enzyme S1P-lyase in tissue cells. Recently, four preclinical observational studies determined S1P levels in serum or plasma of sepsis patients, and all found reduced S1P levels associated with the disease. Based on these findings, this review summarizes S1P-regulated processes pertaining to endothelial functions, discusses the possible use of S1P as a marker and possibilities how to manipulate S1P levels and S1P receptor activation to restore endothelial integrity, dampen the inflammatory host response, and improve organ function in sepsis.
Thirty-two patients were diagnosed as phase Ⅲ silicosis by the local occupational disease prevention and control center. Fifteen patients were type Ⅰ respiratory failure and 17 patients were type Ⅱ. There were 14 cases accepted bilateral sequential lung transplantation and 18 cases accepted single lung transplantation, including 13 cases with right single lung transplantation and 5 cases with left single lung transplantation. Extracorporeal membrane oxygenation was used in 13 patients. Pulmonary function monitoring was performed at 3 months, 6 months, 1 year, and 2 years after lung transplantation. Clinical characteristics were compared using t-test, χ(2) test and Fisher exact test between groups, Kaplan-Meier survival curve and Log-rank test were used to find out the factors affecting survival. Results: All the patients received lung transplantation successfully. One patient died of multiple organ failure, 1 died of sepsis, and 1 succumbed to sudden cardiac death. Twenty-nine patients were discharged from hospital. During follow-up, there were 5 deaths, two patients died of sepsis 7 months postoperatively, 1 died of renal failure 5 months post-transplant, 1 died of sudden cardiac death, and the remaining 1 patient died of bronchiolitis obliterans. Twenty-four patients lived a good quality of life, with survival rates of 90.6% at 3 months, 80.8% at 1 year, 76.7% at 3 years, and 76.7% at 5 years. Significant difference was not observed between single and bilateral lung transplantation about long-term survival rate. During follow-up pulmonary function post-transplant (3 months, 6 months, 1 year, and 2 years) were improved dramatically compared with preoperative level, and patients lived a good quality of life. Conclusion: Lung transplantation is beneficial for patients with phase Ⅲ silicosis, long-term survival is probable.
We also aimed to identify any precipitating factors or events that may trigger these admissions, as well as establish variables that could affect mortality.
We performed a retrospective analysis of kidney transplant recipients admitted to critical care within 1 year after transplant, between January 2009 and December 2013.
Of 1002 kidney transplants, 53 patients (5.3%) were admitted to critical care within 1 year, with patients separated into 2 groups. Group 1 comprised 32 patients (61%) who were admitted immediately postoperatively, mainly from cardiorespiratory derangements with mean stay of 3.7 days (range, 1-34 days) and 0 mortalities. Group 2 comprised 21 patients (39%) who were admitted later in the postoperative period, principally from sepsis-related complications with a mean stay of 18 days (range, 1-101 days). Most patients in group 2 required intensive therapy, including mechanical ventilation and immunosupprression reduction, incurring a hospital mortality rate of 48%. Hemorrhage with reexploration was higher in group 1. Diabetes mellitus, cardiac comorbidity, prolonged stay, nutritional support, nosocomial infections, and multiple organ failure were found at a higher rate in the group 2 patients who died.
The incidence of critical care admissions 1 year after kidney transplant was 5.3%. Most admissions occurred in the early postoperative period, mostly as preemptive measures for cardiorespiratory monitoring and support. This category of admission is potentially preventable with optimization of preoperative treatment. Later admissions were mostly consequential to sepsis-related complications, with patients having a high mortality rate due to multiple organ failure. Clinical management should therefore focus on the prevention of multiple organ failure to improve patient outcomes.
The aim of this study was to assess whether an association exists between the presence of extracellular histones in machine perfusates and deceased donor kidney viability.
Machine perfusates of 390 donation after circulatory death kidneys were analysed for histone concentration and corresponding graft function and survival were assessed.
Extracellular histone concentrations were significantly higher in perfusates of kidneys with posttransplant graft dysfunction (primary non function (PNF) and delayed graft function (DGF)) and were an independent risk factor for DGF (OR=2.152 (1.199-3.863)) and one year graft failure (HR=1.386 (1.037-1.853)), but not for PNF (OR=1.342 (0.900-2.002). One year graft survival was 12% higher in the group with low histone concentrations (p=.008) as compared to the group that contained higher histone concentrations.
This study warrants future studies to probe for a possible role of cytotoxic extracellular histones in organ viability and suggests that quantitation of extracellular histones might contribute to assessment of posttransplant graft function and survival.