S100B and Neuron-Specific Enolase as mortality predictors in patients with severe traumatic brain injury.

OBJECTIVE: To determine temporal profile and prognostic ability of S100B protein and neuron-specific enolase (NSE) for prediction of short/long-term mortality in patients suffering from severe traumatic brain injury (sTBI). METHODS: Ninety-nine patients with sTBI were included in the study. Blood samples were drawn on admission and on subsequent 24, 48, 72, and 96 h. RESULTS: 15.2% of patients died in NeuroCritical Care Unit, and 19.2% died within 6 months of the accident. S100B concentrations were significantly higher in patients who died compared to survivors. NSE levels were different between groups just at 48 h. In the survival group, S100B levels decreased from 1st to 5th sample (p < 0.001); NSE just from 1st to 3rd (p < 0.001) and then stabilized. Values of S100B and NSE in non-survival patients did not significantly vary over the four days post sTBI. ROC-analysis showed that all S100B samples were useful tools for predicting mortality, the best the 72 h sample (AUC 0.848 for discharge mortality, 0.855 for six-month mortality). NSE ROC-analysis indicated that just the 48-h sample predicted mortality (AUC 0.733 for discharge mortality, 0.720 for six-month mortality). CONCLUSION: S100B protein showed higher prognostic capacity than NSE to predict short/long-term mortality in sTBI patients.

S100B protein may detect brain death development after severe traumatic brain injury.

Despite improvements in the process of organ donation and transplants, the number of organ donors is progressively declining in developed countries. Therefore, the early detection of patients at risk for brain death (BD) is a priority for transplant teams seeking more efficient identification of potential donors. In the extensive literature on S100B as a biomarker for traumatic brain injury (TBI), no evidence appears to exist on its prognostic capacity as a predictor of BD after severe TBI. The objective of this study is to assess the value of including acute S100B levels in standard clinical data as an early screening tool for BD after severe TBI. This prospective study included patients with severe TBI (Glasgow Coma Scale score [GCS] ≤ 8) admitted to our Neurocritical Care Unit over a 30 month period. We collected the following clinical variables: age, gender, GCS score, pupillary alterations at admission, hypotension and pre-hospital desaturation, CT scan results, isolated TBI or other related injuries, Injury Severity Score (ISS), serum S100B levels at admission and 24 h post-admission, and a final diagnosis regarding BD. Of the 140 patients studied, 11.4% developed BD and showed significantly higher S100B concentrations (p<0.001). Multivariate analysis showed that bilateral unresponsive mydriasis at admission and serum S100B at 24 h post-admission had odds ratios (ORs) of 21.35 (p=0.005) and 4.9 (p=0.010), respectively. The same analysis on patients with photomotor reflex in one pupil at admission left only the 24 h S100B sample in the model (OR=15.5; p=0.009). Receiver operating characteristics (ROC) curve analysis on this group showed the highest area under the curve (AUC) (0.86; p=0.001) for 24 h S100B determinations. The cut off was set at 0.372 µg/L (85.7% sensitivity, 79.3% specificity, positive predictive value [PPV]=18.7% and negative predictive value [NPV]=98.9%). This study shows that pupillary responsiveness at admission, as well as 24 h serum S100B levels, could serve as screening tools for the early detection of patients at risk for BD after severe TBI.

Red blood cell transfusion in non-bleeding critically ill patients with moderate anemia: is there a benefit?

PURPOSE: This study was undertaken to investigate the efficacy of red blood cell transfusion (RBCT) at reversing the deleterious effects of moderate anemia in critically ill, non-bleeding patients. METHODS: This was a retrospective, pair-matched (ratio 1:1) cohort study. Non-bleeding critically ill patients with moderate anemia (nadir hemoglobin level between 70 and 95 g/l), admitted to the ICU over a 27-month period, were included. Anemic patients were included upon meeting five matching criteria of having the same nadir hemoglobin (±5 g/l), APACHE II score (±5), SOFA score (±2), admission diagnostic group, and age (±5 years). Outcome events occurring over the whole ICU stay and after RBCT were collected. After hospital discharge, all patients had a 2-year follow-up period. RESULTS: Two hundred fourteen non-transfused anemic patients (NTAPs) were successfully matched with 214 transfused anemic patients (TAPs). In addition to the matching criteria, at baseline, both groups were homogenous with respect to multiple comorbidities. Compared with TAPs, NTAPs showed significantly lower rates of hospital mortality (21 vs.13 %, respectively; p < 0.05) and ICU re-admission (7.4 vs. 1.9 %, respectively; p < 0.05). Additionally, NTAPs had significantly lower rates of nosocomial infection (12.9 vs. 6.7 %, respectively; p < 0.05) and acute kidney injury (24.8 vs. 16.7 %, respectively; p < 0.05). Similar results were obtained in subgroup analysis where only more anemic patients (68 matched pairs) or patients with cardiovascular comorbidities (63 matched pairs) were considered. CONCLUSIONS: RBCT does not improve the clinical outcome in non-bleeding critically ill patients with moderate anemia.

Role of early cell-free DNA levels decrease as a predictive marker of fatal outcome after severe traumatic brain injury.

INTRODUCTION: Circulating cell-free DNA levels are increased after trauma injury. This increase is higher since the first hours after trauma and may be related with primary outcome. A sensitive and reliable biomarker for patients at higher risk is needed to identify these patients to initiate early intervention. In this way, circulating DNA may be a possible biological marker after severe TBI. MATERIALS AND METHODS: We investigated DNA plasma concentrations after severe traumatic brain injury and during the next 96 h in the Intensive Care Unit (ICU) by real time PCR. 65 patients suffering severe TBI were included in the study. RESULTS: Cell-free DNA levels were considerably higher in patients samples compared with voluntary control ones. After the following four days we observed a 51% decrease during the first 24h and a 71% fall from 48 h. TBI population was stratified for the primary outcome (survivors/non-survivor) and DNA levels decrease ratio was calculated for the first 48 h. A higher decrease in the survivors from 0 h to 24h compared with the non-survivors was found. A cut-off point of 1.95 ratio was established for the detection of the highest proportions of patients after the TBI that will not survive after the injury with a sensitivity of 70% and specificity of 66%. CONCLUSIONS: In summary we showed that severe TBI is associated with elevated cf-DNA levels and we propose that cf-DNA decrease during the first 24h may predict patient outcome.