6-month Neurological Outcome Research Articles

Amplitude-Integrated Electroencephalography Predicts Outcome in Patients with Coma After Acute Brain Injury.

Prognostication of coma patients after brain injury is important, yet challenging. In this study, we evaluated the predictive value of amplitude-integrated electroencephalography (aEEG) for neurological outcomes in coma patients. From January 2013 to January 2016, 128 coma patients after acute brain injury were prospectively enrolled and monitored with aEEG. The 6-month neurological outcome was evaluated using the Cerebral Performance Category Scale. aEEG monitoring commenced at a median of 7.5 days after coma onset. Continuous normal voltage predicted a good 6-month neurological outcome with a sensitivity of 93.6% and specificity of 85.2%. In contrast, continuous extremely low voltage, burst-suppression, or a flat tracing was correlated with poor 6-month neurological outcome with a sensitivity of 76.5% and specificity of 100%. In conclusion, aEEG is a promising predictor of 6-month neurological outcome for coma patients after acute brain injury.

Low serum Kallistatin level was associated with poor neurological outcome of out-of-hospital cardiac arrest survivors: Proteomics study

Aim of the studyTo identify proteins of which depletion are associated with the poor 6-month neurological outcome of out-of-hospital cardiac arrest survivors. MethodsSeven healthy volunteers and 34 out-of-hospital cardiac arrest survivors admitted to the intensive care unit (ICU) and underwent targeted-temperature management were enrolled. According to the 6-month cerebral performance category (CPC) scale, patients were divided into the good (CPC 1–2) and poor (CPC 3–5) outcome groups. Blood samples were obtained at 0, 24, and 72 h after admission to the ICU. ResultsWith proteomic approaches, we found 23 proteins that showed group-differences between the sera pooled from 7 study groups: healthy volunteers, the good outcome groups (0, 24, and 72 h), and the poor outcome groups (0, 24, and 72 h). We selected 7 candidate proteins of which intensities were different between the good and poor outcome groups (>2-fold change) and excluded 5 proteins related to haemolysis or remaining high abundant proteins. To confirm the 2 identified proteins: retinal dehydrogenase 1 and Kallistatin, we performed enzyme-linked immunosorbent assay with individual serum. Finally, old age (odds ratio = 1.055; 95% confidence interval, 1.002–1.112; p = 0.043) and low serum kallistatin level at 0 h (odds ratio = 0.784; 95% confidence interval, 0.618–0.995; p = 0.046) were independently associated with the poor 6-month neurological outcome. ConclusionThe depletion of serum kallistatin at admission to the ICU was associated with the poor neurological outcome of out-of-hospital cardiac arrest survivors.

Visualizing Cerebrovascular Autoregulation Insults and Their Association with Outcome in Adult and Paediatric Traumatic Brain Injury.

The aim of this study is to assess visually the impact of duration and intensity of cerebrovascular autoregulation insults on 6-month neurological outcome in severe traumatic brain injury. Retrospective analysis of prospectively collected minute-by-minute intracranial pressure (ICP) and mean arterial blood pressure data of 259 adult and 99 paediatric traumatic brain injury (TBI) patients from multiple European centres. The relationship of the 6-month Glasgow Outcome Scale with cerebrovascular autoregulation insults (defined as the low-frequency autoregulation index above a certain threshold during a certain time) was visualized in a colour-coded plot. The analysis was performed separately for autoregulation insults occurring with cerebral perfusion pressure (CPP) below 50 mmHg, with ICP above 25 mmHg and for the subset of adult patients that did not undergo decompressive craniectomy. The colour-coded plots showed a time-intensity-dependent association with outcome for cerebrovascular autoregulation insults in adult and paediatric TBI patients. Insults with a low-frequency autoregulation index above 0.2 were associated with worse outcomes and below -0.6 with better outcomes, with and approximately exponentially decreasing transition curve between the two intensity thresholds. All insults were associated with worse outcomes when CPP was below 50 mmHg or ICP was above 25 mmHg. The colour-coded plots indicate that cerebrovascular autoregulation is disturbed in a dynamic manner, such that duration and intensity play a role in the determination of a zone associated with better neurological outcome.

Can red blood cell distribution width predict outcome after cardiac arrest?

In critically ill patients, high red blood cell distribution width (RDW) values have been associated with increased hospital mortality, but there are no data on the impact of RDW on outcomes of patients resuscitated from cardiac arrest (CA). The aim of this study was to investigate the relationship between RDW and long-term neurologic outcome in CA survivors. We performed a retrospective analysis of an institutional database including all unconscious adult patients admitted to the intensive care unit (ICU) after non-traumatic CA between January 2007 and January 2015. Patients who survived <24 hours were excluded. The RDW (normal values 10.9-13.4%) was obtained daily from the day of admission to day 3. Patients with a cerebral performance category (CPC) score of 3-5 at 3 months were considered to have an unfavourable neurological outcome. Three hundred and ninety patients were included. The ICU mortality rate was 56% (N.=220) and 64% of patients (N.=251) had an unfavorable 3-month neurological outcome. The median RDW on the day of admission was 14% (13.0-15.2%) and remained stable over the observation period. Two hundred and forty-five patients (63%) had a high RDW (>13.4%) on admission. In multivariable logistic regression analysis, older age, absence of bystander cardiopulmonary resuscitation (CPR), a non-cardiac etiology of the arrest, a non-shockable initial rhythm, high adrenaline dose during CPR and high admission RDW levels were independently associated with an unfavorable outcome at 3 months. High RDW values are associated with poor neurological outcome among CA survivors.

Lesions in deep gray nuclei after severe traumatic brain injury predict neurologic outcome.

PurposeThis study evaluates the correlation between injuries to deep gray matter nuclei, as quantitated by lesions in these nuclei on MR T2 Fast Spin Echo (T2 FSE) images, with 6-month neurological outcome after severe traumatic brain injury (TBI).Materials and methodsNinety-five patients (80 males, mean age = 36.7y) with severe TBI were prospectively enrolled. All patients underwent a MR scan within the 45 days after the trauma that included a T2 FSE acquisition. A 3D deformable atlas of the deep gray matter was registered to this sequence; deep gray matter lesions (DGML) were evaluated using a semi-quantitative classification scheme. The 6-month outcome was dichotomized into unfavorable (death, vegetative or minimally conscious state) or favorable (minimal or no neurologic deficit) outcome.ResultsSixty-six percent of the patients (63/95) had both satisfactory registration of the 3D atlas on T2 FSE and available clinical follow-up. Patients without DGML had an 89% chance (P = 0.0016) of favorable outcome while those with bilateral DGML had an 80% risk of unfavorable outcome (P = 0.00008). Multivariate analysis based on DGML accurately classified patients with unfavorable neurological outcome in 90.5% of the cases.ConclusionLesions in deep gray matter nuclei may predict long-term outcome after severe TBI with high sensitivity and specificity.

Targeted Temperature Management for 48 vs 24 Hours and Neurologic Outcome After Out-of-Hospital Cardiac Arrest

International resuscitation guidelines recommend targeted temperature management (TTM) at 33°C to 36°C in unconscious patients with out-of-hospital cardiac arrest for at least 24 hours, but the optimal duration of TTM is uncertain. To determine whether TTM at 33°C for 48 hours results in better neurologic outcomes compared with currently recommended, standard, 24-hour TTM. This was an international, investigator-initiated, blinded-outcome-assessor, parallel, pragmatic, multicenter, randomized clinical superiority trial in 10 intensive care units (ICUs) at 10 university hospitals in 6 European countries. Three hundred fifty-five adult, unconscious patients with out-of-hospital cardiac arrest were enrolled from February 16, 2013, to June 1, 2016, with final follow-up on December 27, 2016. Patients were randomized to TTM (33 ± 1°C) for 48 hours (n = 176) or 24 hours (n = 179), followed by gradual rewarming of 0.5°C per hour until reaching 37°C. The primary outcome was 6-month neurologic outcome, with a Cerebral Performance Categories (CPC) score of 1 or 2 used to define favorable outcome. Secondary outcomes included 6-month mortality, including time to death, the occurrence of adverse events, and intensive care unit resource use. In 355 patients who were randomized (mean age, 60 years; 295 [83%] men), 351 (99%) completed the trial. Of these patients, 69% (120/175) in the 48-hour group had a favorable outcome at 6 months compared with 64% (112/176) in the 24-hour group (difference, 4.9%; 95% CI, -5% to 14.8%; relative risk [RR], 1.08; 95% CI, 0.93-1.25; P = .33). Six-month mortality was 27% (48/175) in the 48-hour group and 34% (60/177) in the 24-hour group (difference, -6.5%; 95% CI, -16.1% to 3.1%; RR, 0.81; 95% CI, 0.59-1.11; P = .19). There was no significant difference in the time to mortality between the 48-hour group and the 24-hour group (hazard ratio, 0.79; 95% CI, 0.54-1.15; P = .22). Adverse events were more common in the 48-hour group (97%) than in the 24-hour group (91%) (difference, 5.6%; 95% CI, 0.6%-10.6%; RR, 1.06; 95% CI, 1.01-1.12; P = .04). The median length of intensive care unit stay (151 vs 117 hours; P < .001), but not hospital stay (11 vs 12 days; P = .50), was longer in the 48-hour group than in the 24-hour group. In unconscious survivors from out-of-hospital cardiac arrest admitted to the ICU, targeted temperature management at 33°C for 48 hours did not significantly improve 6-month neurologic outcome compared with targeted temperature management at 33°C for 24 hours. However, the study may have had limited power to detect clinically important differences, and further research may be warranted. clinicaltrials.gov Identifier: NCT01689077.

Editor's Choice-Progress in the chain of survival and its impact on outcomes of patients admitted to a specialized high-volume cardiac arrest center during the past two decades.

Cardiac arrest (CA) is still associated with high mortality and morbidity. Data on the changes in management and outcomes over a long period of time are limited. Using data from a single emergency department (ED), we assessed changes over two decades. In this single-center observational study, we prospectively included 4133 patients receiving cardiopulmonary resuscitation and being admitted to the ED of a tertiary care hospital between January 1992 and December 2012. There was a significant improvement in both 6-month survival rates (+10.8%; p < 0.001) and favorable neurological outcome (+4.7%; p < 0.001). While the number of witnessed CA cases decreased (-4.7%; p < 0.001) the proportion of patients receiving bystander basic life support increased (+8.3%; p < 0.001). The proportion of patients with initially shockable ECG rhythms remained unchanged, but cardiovascular causes of CA decreased (-9.6%; p < 0.001). Interestingly, the time from CA until ED admission increased (+0.1 hours; p = 0.024). The use of percutaneous coronary intervention and therapeutic hypothermia were significantly associated with survival. Outcomes of patients with CA treated at a specialized ED have improved significantly within the last 20 years. Improvements in every link in the chain of survival were noted.

Time course of cerebrospinal fluid inflammatory biomarkers and relationship to 6-month neurologic outcome in adult severe traumatic brain injury

ObjectiveActivation of the inflammatory cascade is a known pathophysiologic process in severe traumatic brain injury (TBI) with yet non-standardized scientific data regarding relationship to outcome. The understanding of the time course of expression of cerebrospinal fluid (CSF) biomarker levels following severe TBI is an important step toward using these biomarkers to measure injury severity and/or early response to therapeutic interventions. The objective of the current study is to report the time course and values of a battery of CSF inflammatory biomarkers following severe TBI in our reasonably sized patient cohort. Patients and methodsOur patient cohort consists of 32 consented patients, who met the study's inclusion criteria for data collection from 2000 to 2010. The time course and values of a battery of CSF biomarkers (IL-1β, IL-6, TNF-α, IFN-γ, IL-12p70, IL-10, and IL-8) following severe TBI in this patient cohort was characterized. Additionally, the correlation of biomarker concentration with 6-month neurological outcome was assessed. Serial CSF sampling through an external ventricular drain was performed over the first five days following injury. Concentration of a panel of inflammatory biomarkers (IL-1β, IL-6, TNF-α, IFN-γ, IL-12p70, IL-10, and IL-8) were evaluated using Meso Scale Discovery's Multi-Array technology. Glasgow Outcome Scale (GOS) score at six months following injury was dichotomized into poor outcome (GOS 1-3) and favorable outcome (GOS 4-5). Statistical analyses were performed using Kruskal-Wallis test and linear regression analysis. ResultsThe result shows that CSF concentrations of inflammatory biomarkers had a significant association with 6-month neurological outcome (p-values≤0.05 for each marker), with the favorable outcome group having lower concentrations of these biomarkers on average, in comparison to the poor neurologic outcome group over the first five days after TBI. All inflammatory biomarkers decreased to normal levels by post-trauma day 5, except for IL-6 and IL-8. Upregulation and increased expression of key inflammatory markers following severe TBI were significant predictors of worse 6-month neurologic outcome. Additionally, post-trauma day 5 concentrations of IL-6 and IL-8 remained elevated over normal CSF values. ConclusionThe study shows that inflammatory biomarkers in CSF are potential biomarkers of injury severity and progression and/or recovery; they could prove beneficial in the future assessment of injury severity and response to therapy after severe TBI.

Impact of acute kidney injury on patient outcome in out-of-hospital cardiac arrest: a prospective observational study.

Kidney disease after out-of-hospital cardiac arrest (OHCA) is incompletely described. We examined the occurrence of acute kidney injury (AKI) in OHCA patients and impact of AKI, with or without renal replacement therapy (RRT), on 6-month mortality and neurological outcome. Prospective study at Oslo University Hospital, Oslo, Norway. Adult resuscitated comatose OHCA patients treated with targeted temperature management at 33°C for 24 h were included. AKI and chronic kidney disease (CKD) were classified according to the Kidney Disease Improving Global Outcomes (KDIGO) guidelines. Main outcomes were 6-month mortality and good neurological outcome defined as Cerebral Performance Category 1-2. Among 245 included patients (84% males, mean age 61 years), 11 (4%) had previously known CKD and 112 (46%) developed AKI. Overall 6-month outcome revealed that 112 (46%) died and 123 (50%) had good neurological outcome. Compared with no kidney disease, the presence of AKI was significantly associated with 6-month mortality (odds ratio (OR) 3.17, 95% confidence interval (CI) 1.95-5.43, P < 0.001) and good neurological outcome (OR 0.28, 95% CI 0.16-0.48, P < 0.001). Six-month mortality (50 vs. 61%, P = 0.401) and frequency of good neurological outcome (44 vs. 35%, P = 0.417) were not statistically different in AKI patients with or without RRT, also after excluding patients where RRT was withheld due to futility. Kidney disease occurred in about half of patients successfully resuscitated from OHCA. Presence of AKI, but not RRT, was associated with unfavourable 6-month outcome.

Toll-like receptor 4 (TLR4) is correlated with delayed cerebral ischemia (DCI) and poor prognosis in aneurysmal subarachnoid hemorrhage

Toll-like receptor 4 (TLR4) is one of key players in regulation of inflammation. Animal experiments have suggested an important role of TLR4 in the pathophysiology of subarachnoid hemorrhage (SAH). In present study, TLR4 is investigated in clinical SAH patients to explore its clinical significance. 30 patients with aneurysmal subarachnoid hemorrhage (aSAH) and 20 healthy control patients (HC) were enrolled in this prospective study. Blood samples were collected on days 1, 3 and 7 after admission. TLR4 expression level on cell surface of peripheral blood mononuclear cells (PBMCs) was determined by flow cytometry and presented as mean fluorescence intensity (MFI). Patients were clinically assessed every day after admission to monitor the occurrence of delayed cerebral ischemia (DCI). Participants were followed up until completion of 3months after SAH. Functional outcome was defined by modified Rankin score (mRs). Results show that SAH patients presented a significantly higher TLR4 levels on days 1 and 3 post SAH compared to HC; TLR4 levels in SAH patients on day 1 was highest compared with that on days 3 and 7 and in HC. TLR4 of SAH patients on day 7 declined to the level showing no significant difference with that of HC. In patients with Hunt–Hess grades I–III lower TLR4 levels were observed. Patients with DCI showed significantly higher TLR4 levels than those without DCI. High TLR4 levels were statistically significantly associated with poor functional outcome after 3months. Logistic regression analysis showed that TLR4 level on day 1 was independent predictor for DCI and 3-month poor neurological outcome of aneurysmal SAH patients. In summary, admission TLR4 level on PBMCs (day 1) is an independent risk factor to predict the occurrence of DCI and 3-month poor neurological outcome in aneurysmal SAH patients.

Neuron specific enolase and Glasgow motor score remain useful tools for assessing neurological prognosis after out-of-hospital cardiac arrest treated with therapeutic hypothermia

Aim of the studyIdentifying clinical, electrophysiological and biological predictors for 6-month neurological outcome in survivors at day 3 after cardiac arrest (CA) treated with therapeutic hypothermia (TH). MethodsWe conducted a retrospective cohort study of adults comatose after out-of hospital CA treated with TH. All data were collected from medical charts and laboratory files. ResultsBetween January 2010 and March 2013, among the 130 analysed CA survivors, 27 (21%) had a good neurological outcome at 6 months and 103 (79%) had a poor neurological outcome, including 98 deaths. The Glasgow coma score motor response (GCS-M), pupillary reflexes and Neuron Specific Enolase (NSE) were the three best predictors of neurological outcome (P<0.0001). The area under the Receiver Operating Characteristic curve for NSE was 0.92 [0.84–0.99]. ConclusionNSE values, GCS-M scores and pupillary reflexes are the best predictors of poor 6-month outcome after out-of-hospital CA treated with TH. Of these, NSE values have the best-isolated prognostic performance when above 28.8μg/L.

Blood Biomarkers in Moderate-To-Severe Traumatic Brain Injury: Potential Utility of a Multi-Marker Approach in Characterizing Outcome.

Blood biomarkers are valuable tools for elucidating complex cellular and molecular mechanisms underlying traumatic brain injury (TBI). Profiling distinct classes of biomarkers could aid in the identification and characterization of initial injury and secondary pathological processes. This study characterized the prognostic performance of a recently developed multi-marker panel of circulating biomarkers that reflect specific pathogenic mechanisms including neuroinflammation, oxidative damage, and neuroregeneration, in moderate-to-severe TBI patients. Peripheral blood was drawn from 85 isolated TBI patients (n = 60 severe, n = 25 moderate) at hospital admission, 6-, 12-, and 24-h post-injury. Mortality and neurological outcome were assessed using the extended Glasgow Outcome Scale. A multiplex platform was designed on MULTI-SPOT(®) plates to simultaneously analyze human plasma levels of s100 calcium binding protein beta (s100B), glial fibrillary acidic protein (GFAP), neuron specific enolase (NSE), brain-derived neurotrophic factor (BDNF), monocyte chemoattractant protein (MCP)-1, intercellular adhesion molecule (ICAM)-5, and peroxiredoxin (PRDX)-6. Multivariable logistic regression and area under the receiver-operating characteristic curve (AUC) were used to evaluate both individual and combined predictive abilities of these markers for 6-month neurological outcome and mortality after TBI. Unfavorable neurological outcome was associated with elevations in s100B, GFAP, and MCP-1. Mortality was related to differences in six of the seven markers analyzed. Combined admission concentrations of s100B, GFAP, and MCP-1 were able to discriminate favorable versus unfavorable outcome (AUC = 0.83), and survival versus death (AUC = 0.87), although not significantly better than s100B alone (AUC = 0.82 and 0.86, respectively). The multi-marker panel of TBI-related biomarkers performed well in discriminating unfavorable and favorable outcomes in the acute period after moderate-to-severe TBI. However, the combination of these biomarkers did not outperform s100B alone.

Visualizing the pressure and time burden of intracranial hypertension in adult and paediatric traumatic brain injury

To assess the impact of the duration and intensity of episodes of increased intracranial pressure on 6-month neurological outcome in adult and paediatric traumatic brain injury. Analysis of prospectively collected minute-by-minute intracranial pressure and mean arterial blood pressure data of 261 adult and 99 paediatric traumatic brain injury patients from multiple European centres. The relationship of episodes of elevated intracranial pressure (defined as a pressure above a certain threshold during a certain time) with 6-month Glasgow Outcome Scale was visualized in a colour-coded plot. The colour-coded plot illustrates the intuitive concept that episodes of higher intracranial pressure can only be tolerated for shorter durations: the curve that delineates the duration and intensity of those intracranial pressure episodes associated with worse outcome is an approximately exponential decay curve. In children, the curve resembles that of adults, but the delineation between episodes associated with worse outcome occurs at lower intracranial pressure thresholds. Intracranial pressures above 20mmHg lasting longer than 37min in adults, and longer than 8min in children, are associated with worse outcomes. In a multivariate model, together with known baseline risk factors for outcome in severe traumatic brain injury, the cumulative intracranial pressure-time burden is independently associated with mortality. When cerebrovascular autoregulation, assessed with the low-frequency autoregulation index, is impaired, the ability to tolerate elevated intracranial pressures is reduced. When the cerebral perfusion pressure is below 50mmHg, all intracranial pressure insults, regardless of duration, are associated with worse outcome. The intracranial pressure-time burden associated with worse outcome is visualised in a colour-coded plot. In children, secondary injury occurs at lower intracranial pressure thresholds as compared to adults. Impaired cerebrovascular autoregulation reduces the ability to tolerate intracranial pressure insults. Thus, 50mmHg might be the lower acceptable threshold for cerebral perfusion pressure.

Prognostic models in traumatic brain injury

BackgroundPrognostic models are important tools for heterogeneity adjustment in traumatic brain injury (TBI). Prognoses after TBI have been particularly challenging to predict, with limited availability of robust prognostic models. TBI patients are by definition trauma patients, and often treated in the intensive care unit (ICU). Several prognostic models for ICU and trauma patients have been developed, although their applicability in patients with TBI is uncertain. Recently, however, some new prognostic models specifically designed for patients with TBI were introduced. Still, the optimal type of prognostic model in TBI remains unknown.AimThis aims to investigate the applicability of different types of prognostic models in patients with TBI and to develop novel models with enhanced performance to previous models, focusing on long‐ term outcome prediction.MethodsFour patient databases of patients with TBI treated in the ICU were used to validate three TBI specific models, two computerized tomography (CT) scoring systems, one trauma scoring system, and three intensive care scoring systems. Models were validated by assessing their discrimination using area under the curve (AUC), calibration, and explanatory variation. Logistic regression was used for model customization and development. Models were internally validated using a resample bootstrap technique or a split‐sample technique. Primary outcome was 6‐month mortality and unfavorable neurological outcome by the Glasgow Outcome Scale. 30‐day in‐hospital mortality was used for the trauma scoring system.ResultsStudy populations ranged from 342 to 9915 patients. The TBI models showed the best performance with AUCs between 0.80 and 0.85, followed by the intensive care scoring systems and the CT scores with AUCs between 0.68 to 0.80 and 0.63 to 0.70, respectively. Most models showed poor calibration, although good calibration was achieved following customization. The trauma scoring system exhibited modest to good discrimination (AUC 0.76–0.89) for short‐term mortality prediction but poor calibration. Several new prognostic models, with statistically significant superior performance to previous models were created, among them a combined TBI‐ICU model (‘IMPACT‐APACHE’) and a novel CT scoring system (‘The Helsinki CT score’). Using a TBI‐specific model, based on admission characteristics, up to 40% of the patient's final long‐term outcome could be predicted.ConclusionThe TBI models showed superior predictive performance to the intensive care and trauma scoring systems, showing that TBI patients are a highly specific population in the trauma and ICU setting. Thus, the use of a TBI‐specific model is advocated in the setting of TBI. The newly proposed models were found to be significant improvements over previous models, but require external validation to show generalizability.

Predicting Outcome in Traumatic Brain Injury

Early computerized tomography (CT) abnormalities are important predictors of outcome after traumatic brain injury (TBI). To develop a novel CT scoring system (Helsinki CT score) and to compare it with the Marshall CT classification and the Rotterdam CT score in predicting long-term outcome of patients with TBI. Eight hundred sixty-nine consecutive TBI patients were included in this open-cohort, retrospective, single-center study. Logistic regression was used to develop the Helsinki CT score. The scores from the Marshall, Rotterdam, and Helsinki CT scoring methods were added to a clinical model based on age, motor score, and pupils to evaluate their value in predicting outcome. Internal validity was assessed by a bootstrap technique and expressed as area under the curve (AUC). Outcome was 6-month unfavorable neurological outcome and mortality. Variables included in the Helsinki CT score were bleeding type and size, intraventricular hemorrhage, and suprasellar cisterns. In the present data set, the performance of the Helsinki CT score was superior to that of the Marshall CT and Rotterdam CT scores (AUC, 0.74-0.75 vs 0.63-0.70; P < .001). Addition of the Helsinki CT score modestly increased prognostic performance of the clinical model (AUC neurological outcome +0.02 [P = .002]; AUC mortality, +0.01 [P = .21]). In contrast, the Marshall and Rotterdam CT scores were of no additional predictive value to the clinical model (P > .05). Use of the novel Helsinki CT score improved outcome prediction accuracy, and the Helsinki CT score is a feasible alternative to the Rotterdam and Marshall CT systems. External validation of the Helsinki CT score is advocated to show generalizability.

163 Brain Tissue Oxygenation and 3- and 6-month Neurological Outcome in Severe Traumatic Brain Injury

INTRODUCTION: Brain tissue oxygenation (PbtO2) monitoring has been utilized in the severe traumatic brain injury (sTBI) population as an in vivo tool to detect oxygenation changes in the acute injury phase. It has been previously reported that the longer a patient experiences a PbtO2 of = 15 torr, the greater the likelihood of death. The purpose of this study is to assess PbtO2 values and its relationship to 3- and 6-month outcome in adult sTBI. METHODS: Under an approved Internal Review Board protocol, PbtO2 data were prospectively collected on sTBI patients (Glasgow Coma Scale [GCS] score <9) during the acute 5 days following injury. Intensive care unit management included intracranial pressure (ICP) management per Guidelines of sTBI Management; however, PbtO2 was not treated, just monitored. Glasgow Outcome Scale (GOS) score, a measurement of neurologic outcome, was assessed at 3- and 6-months from injury and dichotomized into poor (GOS 1-3) and favorable outcome (GOS 4-5). Statistical analyses were performed using a logistic regression model controlling for age and initial severity of injury. RESULTS: Two hundred fifty-eight adult, sTBI patients with 3- and 6-month outcome were included. The mean age was 38 ± 17 years, with 69% male and a median GCS of 6. Post-trauma day (PTD) 2 PbtO2 data was chosen for analysis to avoid insertional microtrauma and minimize variability of values seen within the first 24 hours of monitoring. Logistic regression resulted in cut-off values of minimum PbtO2 <16.03 and maximum PbtO2 >37.15 being significant for poor 3-month neurological outcome (odds ratio, [OR] 2.46; 95% confidence interval [CI], 1.29-4.68; P = .004; and OR, 2.71; 95% CI, 1.37-5.33; P = .006, respectively). There was no residual significance for 6-month neurological outcome at these same cutoffs; however, PTD2 PbtO2 values in combination for minimum <18.3 and maximum >37.2 were significant predictors of poor outcome (OR, 2.02; 95% CI, 1.11-3.67; P = .02). CONCLUSION: Monitoring of PbtO2 in the adult sTBI population may be predictive of 3-month neurological outcome and provide a target cohort for early rehabilitation efforts. Additional studies are needed to assess the effectiveness of treating PbtO2 values.

Postresuscitation hemodynamics during therapeutic hypothermia after out-of-hospital cardiac arrest with ventricular fibrillation: A retrospective study

Aims of the studyTo evaluate the incidence of postresuscitation myocardial depression (PRMD) and hemodynamical parameters associated with PRMD in patients treated with therapeutic hypothermia (TH) after out-of-hospital cardiac arrest with ventricular fibrillation (OHCA-VF). MethodsAnalysis of hemodynamical data from computerized clinical databases of two academic ICUs during two year period. We analyzed hemodynamical data from a subgroup of patients with pulmonary artery catheter (PAC). We defined PRMD as a cardiac index (CI) less than 1.5l/(minm2) any time during the first 12h and compared clinical variables and hemodynamical parameters in patients with or without PRMD. ResultsOf 120 included patients PAC monitoring was used in 47 (39%). Of 47, 31 (66%, 95% CI 52% to 80%) developed PRMD. There was no difference in urinary output, lactate, mean arterial or central venous pressures or mixed venous saturation between patients with or without PRMD. Low CI was reversed with dobutamine infusion. Presence or absence PRMD was not associated with 6-month neurological outcome. ConclusionTwo-thirds of the OHCA-VF patients develops transient postresuscitation myocardial depression not easily detected without monitoring of CI during therapeutic hypothermia. Further controlled studies are warranted to evaluate the value of different hemodynamic targets and monitoring after cardiac arrest in terms of outcome.

Abstract T P7: Endovascular Therapy with Solitaire Flow Restoration Device after Intravenous t-PA versus t-PA Alone for Stroke

Background: Solitaire flow restoration device have showed advantages in comparison with Merci device that is most used in endovascular therapy trials. We compared the effectiveness and safety of the additional Solitaire treatment and intravenous t-PA alone for stroke patients. Subjects and Methods: Consecutive patients with proximal intracranial occlusion who received intra-arterial reperfusion procedures by mechanical recanalization retrievable self-expanding stent (Solitaire group) after IV t-PA were studied. They were compared with patients from our prospective IV t-PA database with middle cerebral artery or basilar artery occlusion (IV group). Arterial occlusions were assessed with computed tomography angiography before IV t-PA treatment. Patients in Solitaire group underwent angiography as soon as possible after IV t-PA, and those with a vascular occlusion received endovascular intervention with Solitaire FR revascularization device. Clinical evaluation was assessed by National Institutes of Health Stroke Scale at baseline, 24 hours, and at discharge. Symptomatic intracranial hemorrhage was defined according to the National Institute of Neurological Disorders and Stroke trial. Functional evaluation was determined by modified Rankin Scale, with functional independence defined by modified Rankin Scale score of 2 at 3 months. Results: Thirty patients in the Solitaire group were compared with 74 patients in the IV group. The mean age was 59.7±12.5 years. 46 patients (44.2%) were women, and baseline median National Institutes of Health Stroke Scale score was 17 (interquartile range, 6). Mean time from symptoms to IV tPA was 151.4±47.9 minutes. More patients had good 3-month neurological outcome with Solitaire than with IV alone (56.7% vs 35.1%, p=0.04). Symptomatic intracranial hemorrhage was similar (Solitaire 6.7% versus IV 5.4%, P =1). Mortality at 3 months was 13.3% in the Solitaire group and 20.3% in the IV group (p=0.57). Conclusions: In this non-randomized study, compared with intravenous t-PA alone, additional Solitaire treatment was associated with better clinical outcome in in stroke patients with proximal intracranial occlusion.

Abstract 223: Failed Intubation Attempt During Emergency Department Resuscitation of Out-of-Hospital Cardiac Arrest Patient

Backgrounds: Endotracheal intubation is a commonly used procedure to secure airway during emergency department (ED) resuscitation of out-of-hospital cardiac arrest (OHCA) patients. However, it can lead to many complications such as airway trauma or esophageal intubation. Currently, it is unknown whether failed intubation attempt has clinically significant impact on prognosis during resuscitation of OHCA patients in ED where multiple airway adjunct and many trained rescuers are available. Methods: An ED OHCA registry of a tertiary hospital extending from 2008 to 2012 were reviewed to identify non-traumatic OHCA patients who were resuscitated on ED arrival. Prehopsital and demographic factors and patient outcomes were retrieved from the registry. Number of failed intubation attempts was assessed from nurse-documented CPR records. Primary outcome was achievement of sustained return of spontaneous circulation (ROSC). Secondary outcomes were survival discharge and 6-month neurologic outcome. Results: 512 non-traumatic OHCA patients with ED intubation attempt during resuscitation were included. Failed intubation attempt was present in 77 patients and there was no significant difference in demographic or prehospital factors between those with and without it. With failed intubation attempt, the unadjusted and adjusted odds ratios (ORs) for achieving sustained ROSC was 0.62 (95% confidence interval [CI], 0.38-1.01) and 0.51 (95% CI, 0.29-0.89), respectively. In a propensity-matched sample, the adjusted OR was 0.82 (95% CI, 0.69-0.97). However, no significant difference in long-term outcomes was found in any of the analyses. Conclusion: Failed intubation attempt in ED was an independent risk factor for resuscitation failure in ED OHCA patients.

Editorial: Intracranial pressure monitoring for brain injury

Zeng and colleagues examine the impact of treatment based on monitored intracranial pressure (ICP) versus that delivered without monitoring on both 6-month neurologic outcome (Glasgow Outcome Scale score) and renal function.5 They report significantly better recovery and less renal dysfunction in monitored patients managed in accordance with the Brain Trauma Foundation guidelines. Unfortunately, these authors do not present data sufficient to support their claim of improved outcome. Neither do they securely establish that ICP monitoring would be associated with less renal failure if this study were repeated elsewhere. Patients were parsed into monitored versus non-monitored groups according to the Brain Trauma Foundation’s recommendations as to whom published evidence suggests should be monitored. These criteria include CT imaging characteristics, age, admission Glasgow Coma Scale [GCS] motor score, and history or presence of hypotension. By definition, then, these are dissimilar groups, and it is the authors’ responsibility to quantify and control the differences in their analysis. Unfortunately, these data were not presented; rather, the groups were deemed demographically similar based on examination of age, total admission GCS score, and sex alone. It remains unproven, and highly unlikely, that these groups are similar enough in terms of outcome-relevant demographic characteristics to allow attributing differences in outcome to ICPmonitor–based management. In our recent randomized controlled trial (RCT),1 when such variables were studied and controlled, we found no difference in outcome between monitored and non-monitored groups. Regarding renal toxicity, the major risk in trauma patients, particularly those receiving hyperosmotic agents, is hypovolemia. Given that Zeng et al. found (as did we in our RCT) that ICP monitoring is associated with significantly decreased use of brain-specific therapies, including mannitol, patients managed without monitoring were at increased risk of negative fluid balance and renal hypoperfusion. In contrast to our findings, this risk was associated with what they called increased acute kidney injury (AKI). Unfortunately, they did not clearly define AKI and their reference to that definition4 does not provide one. The currently accepted definition of AKI2,3 would not support their reported AKI incidences. Furthermore, lack of information as to daily fluid balance or fractional excretion of sodium make it difficult to believe that the group differences in the renal data that they present are not simply due to lack of volume replacement to balance iatrogenic diuresis. In our RCT, the management protocol for all included patients required close attention to maintaining normovolemia, and our incidence of renal dysfunction was globally low and not related to treatment group (3% and 4%, for monitored versus non-monitored patients [p = 1.0], presented in Table 10b in the online supplements to the RCT available at NEJM.org).1 The use of ICP monitoring remains a critical aspect of the care of patients with severe traumatic brain injury despite the body of recent evidence suggesting that our interpretation and management algorithms need refinement based on clinical research. However, the risk of confounding is very high in such studies and requires meticulous prospective study design and data collection, shortcomings in which greatly inhibit the value of this study. (http://thejns.org/doi/abs/10.3171/2013.5.JNS13254)