Comparison of the predictive performance of the BIG,TRISS, and PS09 score in an adult trauma population derived from multiple international trauma registries

Background

The BIG score (Admission base deficit (B), International normalized ratio (I), and Glasgow Coma Scale (G)) has been shown to predict mortality on admission in pediatric trauma patients. The objective of this study was to assess its performance in predicting mortality in an adult trauma population, and to compare it with the existing Trauma and Injury Severity Score (TRISS) and probability of survival (PS09) score.

Materials and methods

A retrospective analysis using data collected between 2005 and 2010 from seven trauma centers and registries in Europe and the United States of America was performed. We compared the BIG score with TRISS and PS09 scores in a population of blunt and penetrating trauma patients. We then assessed the discrimination ability of all scores via receiver operating characteristic (ROC) curves and compared the expected mortality rate (precision) of all scores with the observed mortality rate.

Results

In total, 12,206 datasets were retrieved to validate the BIG score. The mean ISS was 15 ± 11, and the mean 30-day mortality rate was 4.8%. With an AUROC of 0.892 (95% confidence interval (CI): 0.879 to 0.906), the BIG score performed well in an adult population. TRISS had an area under ROC (AUROC) of 0.922 (0.913 to 0.932) and the PS09 score of 0.825 (0.915 to 0.934). On a penetrating-trauma population, the BIG score had an AUROC result of 0.920 (0.898 to 0.942) compared with the PS09 score (AUROC of 0.921; 0.902 to 0.939) and TRISS (0.929; 0.912 to 0.947).

Conclusions

The BIG score is a good predictor of mortality in the adult trauma population. It performed well compared with TRISS and the PS09 score, although it has significantly less discriminative ability. In a penetrating-trauma population, the BIG score performed better than in a population with blunt trauma. The BIG score has the advantage of being available shortly after admission and may be used to predict clinical prognosis or as a research tool to risk stratify trauma patients into clinical trials.     

Akzidentelle Hypothermie

Uncertainty exists on how to treat patients suffering from accidental hypothermia and on the optimal transport decisions. The aim of this review is to provide an updated evidence-based reference for the pre-hospital and in-hospital management of patients with accidental hypothermia and for the transport decisions required to facilitate treatment. Advances in the efficiency and availability of rewarming techniques have improved the prognosis for patients presenting with hypothermia. For hypothermic patients with a core body temperature ≥?28?°C without cardiac instability there is increasing evidence to support the use of active external and minimally invasive rewarming techniques (e.g. chemical, electrical or forced air heating packs, blankets and warm parenteral fluids). Hypothermic patients with cardiac instability (i.e. systolic blood pressure <?90 mmHg, ventricular arrhythmia and core body temperature <?28?°C) should be rewarmed with active external and minimally invasive rewarming techniques in a hospital which also has circulation substituting venous-arterial extracorporeal membrane oxygenation (VA-ECMO) and cardiopulmonary bypass (CBP) facilities. In cardiac arrest patients VA-ECMO may be a better treatment option than CBP and survival rates of 100?% can be achieved compared to ~?10?% with traditional methods (e.g. body cavity lavage). Early transport to a hospital appropriately equipped for rewarming has the potential to decrease complication rates and improve survival.     

The effect of a silane coupling agent on the bond strength of bone cement and cobalt-chrome alloy

Debonding of the cement-implant interface has been hypothesized to be the leading initial indicator of failed total hip prostheses. Many attempts have been made to increase the bond strength of this interface by precoating the implant, increasing the implant's surface roughness, and creating macro-grooves or channels on the implant. However, each of these approaches introduces new complications. This study introduces a unique silane coupling agent used to chemically bond the bone cement to the implant. Cylindrical cobalt-chrome samples were treated with the silane coupling agent, bonded to polymethylmethacrylate, and pushed out to failure. The mean shear strengths were compared to the failure strengths of untreated samples. Half of the specimens were tested immediately following cement curing, and the other half were tested after immersion in saline solution for 60 days. The mean shear strength of the silane-coated samples ranged from 18.2 to 24.1 MPa, and the mean shear strength of the uncoated samples ranged from 7.6 to 15.0 MPa. The increase in strength following silane coating noted in this study may increase the longevity of the implant by decreasing debonding at the interface and, therefore, subsequent failure due to loosening.     

Vitamin K status in cystic fibrosis

Appearance of PIVKA-II (protein induced by vitamin K absence-II) in serum is a biochemical sign of insufficient vitamin K-dependent carboxylation of prothrombin. Plasma concentrations of PIVKA-II and vitamin K1 were determined in 24 children with cystic fibrosis. Eight were supplemented with vitamin K1. The purpose of the study was to determine the occurrence of vitamin K deficiency in cystic fibrosis and to evaluate the effect of vitamin K supplementation. PIVKA-II was detectable in only one unsupplemented child. In this patient, the concentration of vitamin K1 was below the limit of detection of 60 ng/l. Vitamin K1 levels in the other unsupplemented children were normal (mean 476 ng/l = 1 mmol/l). The supplemented patients showed extremely high levels of vitamin K1 (mean 22445 ng/l = 50 nmol/l). In conclusion, vitamin K deficiency occurs infrequently in cystic fibrosis. Checking the coagulation system is advised, but routine vitamin K supplementation is not recommended. If additional vitamin K is needed, the starting dose should not exceed 1 mg daily.     

Recurrence of atrial tachyarrhythmias in implantable cardioverter-defibrillator recipients

BACKGROUND: Because the natural history of atrial tachyarrhythmia (AT) is not known in patients with implantable cardioverter-defibrillators (ICDs) but without device-based atrial therapies, we aimed to describe the characteristics and recurrence of AT in such patients. METHODS: In this multicenter trial, 269 patients with standard indications for ICD placement and 2 episodes of AT in the preceding year received a dual-chamber ICD capable of logging AT. Patients were randomly assigned to 3-month periods of atrial therapies "on" or "off." This analysis considered only the 118 patients with atrial therapies programmed off at ICD placement. RESULTS: Fifty-eight patients (49%) had at least 1 AT episode longer than 1 minute, and 21 (18%) had at least 1 prolonged episode (>24 hours). The median episode frequency for each patient (episodes per month) was 1.8 episodes longer than 1 minute, 0.8 longer than 1 hour, and 0 longer than 24 hours. The median AT burden was 12.2 hours per month. CONCLUSIONS: Patients with standard ICD indications and history of AT have infrequent episodes, frequent short episodes, or prolonged episodes of AT-atrial fibrillation. However, the clinical characteristics examined did not distinguish among the groups. Improved diagnostic tools may help identify patients at risk for development of AT, thereby allowing specific therapies to be targeted to each group of patients.     

Mutations in the genes KCND2 and KCND3 encoding the ion channels Kv4.2 and Kv4.3, conducting the cardiac fast transient outward current (ITO,f), are not a frequent cause of long QT syndrome

BACKGROUND: Long QT syndrome (LQTS) is a hereditary cardiac arrhythmogenic disorder characterized by prolongation of the QT interval in the electrocardiogram, torsades de pointes arrhythmia, and syncopes and sudden death. LQTS is caused by mutations in ion channel genes. However, only in half of the families is it possible to identify mutations in one of the seven known LQTS genes, why further genetic heterogeneity is expected. The genes KCND2 and KCND3, encoding the alpha-subunits of the voltage-gated potassium channels Kv4.2 and Kv4.3 conducting the fast transient outward current (I(TO,f)) of the cardiac action potential (AP) in the myocardium, have been associated with prolongation of AP duration and QT prolongation in murine models. METHODS: KCND2 and KCND3 were examined for mutations using single-strand conformation polymorphism (SSCP) analysis in 43 unrelated LQTS patients, where mutations in the coding regions of known LQTS genes had been excluded. RESULTS: Seven single nucleotide polymorphismsm (SNPs) were found, two exonic SNPs in KCND2 and three exonic and two intronic in KCND3. None of the five exonic SNPs had coding effect. All seven SNPs are considered normal variants. CONCLUSION: The data suggest that mutations in KCND2 and KCND3 are not a frequent cause of long QT syndrome.     

Meconium induced IL-8 production and intratracheal albumin alleviated lung injury in newborn pigs

We have recently shown that albumin added to meconium before intratracheal instillation in newborn pigs limits detrimental effect on the lungs and reduces increase of IL-8. The aim of this study was to test the effect of albumin instillation as rescue treatment in meconium aspiration syndrome (MAS). MAS was induced in hypoxic piglets by lung instillation of meconium (MAS I = 675 mg/kg, n=12; MAS II=540 mg/kg, n=14). Morbidity and mortality differed (MAS I, dead=7/12; MAS II, dead=5/14). MAS groups were randomized to postmeconium instillation of either bovine albumin (30%, 1.4 mL/kg; MAS I, n=6; MAS II, n=7) or isotonic saline (9 mg/mL, 1.4 mL/kg; MAS I, n=6; MAS II, n=7). The controls (n=4) were tested by sequential instillation of saline (9 mg/mL, 5 mL/kg) and albumin (30%, 1.4 mL/kg). Lung function and gas exchange deteriorated significantly after instillation of meconium [oxygenation index (OI): MAS I, +814%; MAS II, +386%; ventilation index (VI): MAS I, +256%; MAS II, +162%; compliance: MAS I, -53%; MAS II, -44%]. Increases of tracheal IL-8 correlated to deterioration of lung function were 10- (MAS I) and 5-fold (MAS II) (p <0.001). Lung compliance was higher in albumin instillation versus saline instillation (MAS I, p=0.008; MAS II, p=0.002). Albumin did not influence intergroup differences in IL-8, hemodynamics, OI, or VI. MAS-induced IL-8 increases correlated with deterioration of lung function (OI, VI, and compliance). Rescue treatment with albumin in meconium aspiration improved lung compliance in piglets and may represent a new therapeutic approach to MAS.     

Role of tumour necrosis factor gene polymorphisms (-308 and -238) in breast cancer susceptibility and severity

Introduction  

Genetic polymorphisms in the promoter region of the tumour necrosis factor (TNF) gene can regulate gene expression and have been associated with inflammatory and malignant conditions. We have investigated two polymorphisms in the promoter of the TNF gene (-308 G>A and -238 G>A) for their role in breast cancer susceptibility and severity by means of an allelic association study.