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Activation of the kynurenine pathway (KP) has been shown to predict outcome in cardiac arrest (CA) patients. We validated these findings in a Swiss cohort.We measured admission tryptophan and kynurenine levels in 270 consecutive CA patients (38 in-hospital CA) and investigated associations with in-hospital mortality and neurological outcome at hospital discharge.120 of 270 (44%) patients died in the hospital. Compared to survivors, non-survivors showed higher median initial kynurenine levels (5.28 μmol/l [IQR 2.91 to 7.40] vs 3.58 μmol/l [IQR 2.47 to 5.46]; p 0.001) and a higher median kynurenine/tryptophan ratio (0.10 μmol/l [IQR 0.07 to 0.17] vs 0.07 μmol/l [IQR 0.05 to 0.1]; p 0.001). In a model adjusted for age, gender and comorbidities, kynurenine (OR 1.16, 95% CI 1.05 to 1.27; p = 0.001) and kynurenine/tryptophan ratio (OR 1.19, 95% CI 1.08 to 1.31; p = 0.003) were significantly associated with mortality. Results were similar for neurological outcome.Our findings validate a previous study and show associations of the activation of the KP with unfavorable outcomes after CA. Future studies should evaluate whether therapeutic modulation of the KP may impact clinical outcomes after CA.

IMPORTANCE: Data on long-term survival beyond 12 months after out-of-hospital cardiac arrest (OHCA) of a presumed cardiac cause are scarce. OBJECTIVE: To investigate the long-term survival of adult patients after surviving the initial hospital stay for an OHCA. DATA SOURCES: A systematic search of the EMBASE and MEDLINE databases was performed from database inception to March 25, 2021. STUDY SELECTION: Clinical studies reporting long-term survival after OHCA were selected based on predefined inclusion and exclusion criteria according to a preregistered study protocol. DATA EXTRACTION AND SYNTHESIS: Patient data were reconstructed from Kaplan-Meier curves using an iterative algorithm and then pooled to generate survival curves. As a separate analysis, an aggregate data meta-analysis was performed. MAIN OUTCOMES AND MEASURES: The primary outcome was long-term survival (>12 months) after OHCA for patients surviving to hospital discharge or 30 days after OHCA. RESULTS: The search identified 15 347 reports, of which 21 studies (11 800 patients) were included in the Kaplan-Meier–based meta-analysis and 33 studies (16 933 patients) in an aggregate data meta-analysis. In the Kaplan-Meier–based analysis, the median survival time for patients surviving to hospital discharge was 5.0 years (IQR, 2.3-7.9 years). The estimated survival rates were 82.8% (95% CI, 81.9%-83.7%) at 3 years, 77.0% (95% CI, 75.9%-78.0%) at 5 years, 63.9% (95% CI, 62.3%-65.4%) at 10 years, and 57.5% (95% CI, 54.8%-60.1%) at 15 years. Compared with patients with a nonshockable initial rhythm, patients with a shockable rhythm had a lower risk of long-term mortality (hazard ratio, 0.30; 95% CI, 0.23-0.39; P

Background A recent study found serum neurofilament light chain (NfL) levels to be strongly associated with poor neurological outcome in patients after cardiac arrest. Our aim was to confirm these findings in an independent validation study and to investigate whether NfL improves the prognostic value of two cardiac arrest-specific risk scores. Methods This prospective, single-center study included 164 consecutive adult after out-of-hospital cardiac arrest (OHCA) patients upon intensive care unit admission. We calculated two clinical risk scores (OHCA, CAHP) and measured NfL on admission within the first 24 h using the single molecule array NF-light® assay. The primary endpoint was neurological outcome at hospital discharge assessed with the cerebral performance category (CPC) score. Results Poor neurological outcome (CPC > 3) was found in 60% (98/164) of patients, with 55% (91/164) dying within 30 days of hospitalization. Compared to patients with favorable outcome, NfL was 14-times higher in patients with poor neurological outcome (685 ± 1787 vs. 49 ± 111 pg/mL), with an adjusted odds ratio of 3.4 (95% CI 2.1 to 5.6, p p p p p Conclusions Admission NfL was a strong outcome predictor and significantly improved two clinical risk scores regarding prognostication of neurological outcome in patients after cardiac arrest. When confirmed in future outcome studies, admission NfL should be considered as a standard laboratory measures in the evaluation of OHCA patients.

Objectives Prior research found the gut microbiota-dependent and pro-atherogenic molecule trimethylamine-N-oxide (TMAO) to be associated with cardiovascular events as well as all-cause mortality in different patient populations with cardiovascular disease. Our aim was to investigate the prognostic value of TMAO regarding clinical outcomes in patients after out-of-hospital cardiac arrest (OHCA). Methods We included consecutive OHCA patients upon intensive care unit admission into this prospective observational study between October 2012 and May 2016. We studied associations of admission serum TMAO with in-hospital mortality (primary endpoint), 90-day mortality and neurological outcome defined by the Cerebral Performance Category (CPC) scale. Results We included 258 OHCA patients of which 44.6% died during hospitalization. Hospital non-survivors showed significantly higher admission TMAO levels (μmol L−1) compared to hospital survivors (median interquartile range (IQR) 13.2 (6.6–34.9) vs. 6.4 (2.9–15.9), p Conclusions In patients after OHCA, TMAO levels were independently associated with in-hospital mortality and other adverse clinical outcomes and may help to improve prognostication for these patients in the future. Whether TMAO levels can be influenced by nutritional interventions should be addressed in future studies.

Background With advances in critical care and organ donation, diagnosis of brain death is gaining importance. We aimed to assess potential brain death confounders from the literature, elucidating clinical presentation and diagnostic approaches in these cases. Methods PubMed and Embase were screened using 37 predefined search terms to identify suitable articles reporting cases, case series, or cohort studies in adults. Results Out of 4769 articles, 40 case reports or case series describing 45 patients with 19 critical conditions were identified. Mortality was 11% and full recovery 33%. Intoxications (42%; mainly anti-seizure drugs and baclofen) and polyneuritis (37%) were most frequent. Brainstem reflex tests were reported in 96%, apnoea test in 16% and ancillary tests in all but one patient. Full recovery mainly occurred with intoxications. Quality of evidence regarding frequency of confounders is very low and risk of bias high. Conclusions Brain death confounders are infrequently reported and formal studies are lacking. Mainly younger patients with polyneuritis and intoxications are described. As outcome, especially in the latter, is often favourable, high awareness and strict adherence to guidelines is crucial. The importance of identifying pathologies compatible with extensive and irreversible brain damage before proceeding to diagnostic tests should be emphasized.

Introduction Intensive care unit patients are at risk for post-intensive care syndrome (PICS), which includes psychological, physical and/or cognitive sequelae after their hospital stay. Our aim was to investigate PICS in adult patients with out-of-hospital cardiac arrest (OHCA). Methods In this prospective observational cohort study, we assessed risks for PICS at 3 and 12-month follow-up within the following domains: a) physical impairment (EuroQol [EQ-5D-3L]), b) cognitive functioning (Cerebral Performance Category [CPC] score >1, modified Rankin Scale [mRS] >2) and c) psychological burden (Hospital Anxiety and Depression Scale [HADS], Impact of Event Scale-Revised [IES-R]). Results At 3 months, 69/139 patients (50%) met the definition of PICS including 37% in the physical domain, 25% in the cognitive domain and 13% in the psychological domain. Intubation (OR 2.3, 95%CI 1.1 to 5,0 p = 0.03), sedatives (OR 3.4, 95%CI 1 to 11, p = 0.045), mRS at discharge (OR 4.3, 95%CI 1.70 to 11.01, p = 0.002), CPC at discharge (OR 3.3, 95%CI 1.4 to 7.6, p = 0.005) and post-discharge work loss (OR 13.4, 95%CI 1.7 to 107.5, p = 0.014) were significantly associated with PICS. At 12 months, 52/110 (47%) patients had PICS, which was associated with prolonged duration of rehabilitation, higher APACHE scores, and higher mRS and CPC scores at hospital discharge. Conclusions Nearly half of long-term OHCA survivors show PICS after 3 and 12 months. These high numbers call for more emphasis on appropriate screening and treatment in this patient population. Future studies should evaluate whether early identification of these patients enables preventive strategies and treatment options.

BackgroundDue to the dramatic measures accompanying isolation and the general uncertainty and fear associated with COVID-19, patients and relatives may be at high risk for adverse psychological outcomes. Until now there has been limited research focusing on the prevalence of psychological distress and associated factors in COVID-19 patients and their relatives. The objective of our study was to assess psychological distress in COVID-19 patients and their relatives 30 days after hospital discharge.MethodsIn this prospective observational cohort study at two Swiss tertiary-care hospitals we included consecutive adult patients hospitalized between March and June 2020 for a proven COVID-19 and their relatives. Psychological distress was defined as symptoms of anxiety and/or depression measured with the Hospital Anxiety and Depression Scale (HADS), i.e., a score of ≥8 on the depression and/or anxiety subscale. We further evaluated symptoms of post-traumatic stress disorder (PTSD), defined as a score of ≥1.5 on the Impact of Event Scale-Revised (IES-R).ResultsAmong 126 included patients, 24 (19.1%) had psychological distress and 10 (8.7%) had symptoms of PTSD 30 days after hospital discharge. In multivariate logistic regression analyses three factors were independently associated with psychological distress in patients: resilience (OR 0.82; 95%CI 0.71 to 0.94; p = 0.005), high levels of perceived stress (OR 1.21; 95%CI 1.06 to 1.38; p = 0.006) and low frequency of contact with relatives (OR 7.67; 95%CI 1.42 to 41.58; p = 0.018). The model showed good discrimination, with an area under the receiver-operating characteristic curve (AUC) of 0.92. Among 153 relatives, 35 (22.9%) showed symptoms of psychological distress, and 3 (2%) of PTSD. For relatives, resilience was negatively associated (OR 0.85; 95%CI 0.75 to 0.96; p = 0.007), whereas perceived overall burden caused by COVID-19 was positively associated with psychological distress (OR 1.72; 95%CI 1.31 to 2.25; pConclusionA relevant number of COVID-19 patients as well as their relatives exhibited psychological distress 30 days after hospital discharge. These results might aid in development of strategies to prevent psychological distress in COVID-19 patients and their relatives.

Objective To characterize a critically ill cohort with status epilepticus (SE) by the illness severity scoring systems SAPS II (Simplified Acute Physiology Score II), APACHE II (Acute Physiology and Chronic Health Evaluation II), and SOFA (Sequential Organ Failure Assessment), and to compare their performance with the STESS (Status Epilepticus Severity Score) for outcome prediction. Methods The prospective cohort study was carried out at the University Hospital Basel, a Swiss tertiary academic medical care center. Consecutive adult SE patients hospitalized in the intensive care units from 2011 to 2016 were included. Illness severity scores and additional clinical data were recorded. Logistic regression models using automated variable selection were applied to identify scores associated with no return to functional and neurological baseline and death. Measures of discrimination and calibration were assessed. Results Among 184 patients, 33% returned to baseline. Median scores of the illness severity scores were within the lowest third of the possible scoring ranges, and all differed significantly between patients with and without return to baseline. The areas under the receiver operating curves for the prediction of no return to baseline and death ranged from 0.64 to 0.73, with the highest value for the STESS predicting no return to baseline. Measures of calibration revealed adequate model fit for all analyses. Among integral components of the scoring systems, only the Glasgow Coma Scale (GCS) differed significantly between patients with and without return to baseline. In multivariable analyses, decreasing GCS and increasing STESS had the strongest associations (odds ratio [OR] = 0.84, 95% confidence interval [CI] = 0.77-0.93 and OR = 1.34, 95% CI = 1.05-1.68, respectively) with no return to baseline independent of all other scoring systems, whereas the APACHE II revealed the strongest association with death (OR = 1.15, 95% CI = 1.06-1.25). Significance Although complex illness severity scoring systems in SE patients facilitate benchmarking and comparisons with other severely ill patient cohorts, they offer no advantages over the STESS and GCS regarding prediction of no return to baseline.

Preventive strategies against diagnostic errors require the knowledge of underlying mechanisms. We examined the effects of a wrong a priori diagnosis on diagnostic accuracy of a focussed assessment in an acute myocardial infarction scenario. One-hundred-and-fifty-six medical students (cohort 1) were randomized to three study arms differing in the a priori diagnosis revealed: no diagnosis (control group), myocardial infarction (correct diagnosis group), and pulmonary embolism (wrong diagnosis group). Forty-four physicians (cohort 2) were randomized to the control group and the wrong diagnosis group. Primary endpoint was the participants’ final presumptive diagnosis. Among students, the correct diagnosis of an acute myocardial infarction was made by 48/52 (92%) in the control group, 49/52 (94%) in the correct diagnosis group, and 14/52 (27%) in the wrong diagnosis group (p &lt, 0.001 vs. both other groups). Among physicians, the correct diagnosis was made by 20/21 (95%) in the control group and 15/23 (65%) in the wrong diagnosis group (p = 0.023). In the wrong diagnosis group, 31/52 (60%) students and 6/23 (19%) physicians indicated their initially given wrong a priori diagnosis pulmonary embolism as final diagnosis. A wrong a priori diagnosis significantly increases the likelihood of a diagnostic error during a subsequent patient encounter.

BACKGROUND End-of-life practices vary among intensive care units (ICUs) worldwide. Differences can result in variable use of disproportionate or non-beneficial life-sustaining interventions across diverse world regions. This study investigated global disparities in end-of-life practices. METHODS In this prospective, multinational, observational study, consecutive adult ICU patients who died or had a limitation of life-sustaining treatment (withholding or withdrawing life-sustaining therapy and active shortening of the dying process) during a 6-month period between Sept 1, 2015, and Sept 30, 2016, were recruited from 199 ICUs in 36 countries. The primary outcome was the end-of-life practice as defined by the end-of-life categories: withholding or withdrawing life-sustaining therapy, active shortening of the dying process, or failed cardiopulmonary resuscitation (CPR). Patients with brain death were included in a separate predefined end-of-life category. Data collection included patient characteristics, diagnoses, end-of-life decisions and their timing related to admission and discharge, or death, with comparisons across different regions. Patients were studied until death or 2 months from the first limitation decision. FINDINGS Of 87 951 patients admitted to ICU, 12 850 (14·6%) were included in the study population. The number of patients categorised into each of the different end-of-life categories were significantly different for each region (p

(1) Background: In patients with shock, the L-arginine nitric oxide pathway is activated, causing an elevation of nitric oxide, asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) levels. Whether these metabolites provide prognostic information in patients after out-of-hospital cardiac arrest (OHCA) remains unclear. (2) Methods: We prospectively included OHCA patients, recorded clinical parameters and measured plasma ADMA, SDMA and Arginine levels by liquid chromatography tandem mass spectrometry (LC-MS). The primary endpoint was 90-day mortality. (3) Results: Of 263 patients, 130 (49.4%) died within 90 days after OHCA. Compared to survivors, non-survivors had significantly higher levels of ADMA and lower Arginine and Arginine/ADMA ratios in univariable regression analyses. Arginine levels and Arginine/ADMA ratio were significantly associated with 90-day mortality (OR 0.51 (95%CI 0.34 to 0.76), p &lt, 0.01 and OR 0.40 (95%CI 0.26 to 0.61), p &lt, 0.001, respectively). These associations remained significant in several multivariable models. Arginine/ADMA ratio had the highest predictive value with an area under the curve (AUC) of 0.67 for 90-day mortality. Results for secondary outcomes were similar with significant associations with in-hospital mortality and neurological outcome. (4) Conclusion: Arginine and Arginine/ADMA ratio were independently associated with 90-day mortality and other adverse outcomes in patients after OHCA. Whether therapeutic modification of the L-arginine-nitric oxide pathway has the potential to improve outcome should be evaluated.

Guidelines recommend a ‘do-not-resuscitate’ (DNR) code status for inpatients in which cardiopulmonary resuscitation (CPR) attempts are considered futile because of low probability of survival with good neurological outcome. We retrospectively assessed the prevalence of DNR code status and its association with presumed CPR futility defined by the Good Outcome Following Attempted Resuscitation score and the Clinical Frailty Scale in patients hospitalised in the Divisions of Internal Medicine and Traumatology/Orthopedics at the University Hospital of Basel between September 2018 and June 2019. The definition of presumed CPR futility was met in 467 (16.2%) of 2889 patients. 866 (30.0%) patients had a DNR code status. In a regression model adjusted for age, gender, main diagnosis, nationality, language and religion, presumed CPR futility was associated with a higher likelihood of a DNR code status (37.3% vs 7.1%, adjusted OR 2.99, 95% CI 2.31 to 3.88, p

Background: Studies have suggested that taurine may have neuro- and cardio-protective functions, but there is little research looking at taurine levels in patients after out-of-hospital cardiac arrest (OHCA). Our aim was to evaluate the association of taurine with mortality and neurological deficits in a well-defined cohort of OHCA patients. Methods: We prospectively measured serum taurine concentration in OHCA patients upon admission to the intensive care unit (ICU) of the University Hospital Basel (Switzerland). We analyzed the association of taurine levels and in-hospital mortality (primary endpoint). We further evaluated neurological outcomes assessed by the cerebral performance category scale. We calculated logistic regression analyses and report odds ratios (OR) and 95% confidence intervals (CI). We calculated different predefined multivariable regression models including demographic variables, comorbidities, initial vital signs, initial blood markers and resuscitation measures. We assessed discrimination by means of area under the receiver operating curve (ROC). Results: Of 240 included patients, 130 (54.2%) survived until hospital discharge and 110 (45.8%) had a favorable neurological outcome. Taurine levels were significantly associated with higher in-hospital mortality (adjusted OR 4.12 (95%CI 1.22 to 13.91), p = 0.02). In addition, a significant association between taurine concentration and a poor neurological outcome was observed (adjusted OR of 3.71 (95%CI 1.13 to 12.25), p = 0.03). Area under the curve (AUC) suggested only low discrimination for both endpoints (0.57 and 0.57, respectively). Conclusion: Admission taurine levels are associated with mortality and neurological outcomes in OHCA patients and may help in the risk assessment of this vulnerable population. Further studies are needed to assess whether therapeutic modulation of taurine may improve clinical outcomes after cardiac arrest.

There is interest in novel blood markers to improve risk stratification in patients presenting with cardiac arrest. We assessed associations of different plasma sphingomyelin concentrations and neurological outcome in patients with cardiac arrest. In this prospective observational study, adult patients with cardiac arrest were included upon admission to the intensive care unit (ICU). We studied associations of admission plasma levels of 15 different sphingomyelin species with neurological outcome at hospital discharge (primary endpoint) defined by the modified Rankin Scale by the calculation of univariable and multivariable logistic regression models adjusted for age, gender, and clinical shock markers. We included 290 patients (72% males, median age 65 years) with 162 (56%) having poor neurological outcome at hospital discharge. The three sphingomyelin species SM C24:0, SM(OH) C22:1, and SM(OH) C24:1 were significantly lower in patients with poor neurological outcome compared to patients with favorable outcome with areas under the curve (AUC) of 0.58, 0.59, and 0.59. SM(OH) C24:1 was independently associated with poor neurological outcome in a fully-adjusted regression model (adjusted odds ratio per log-transformed unit increase in SM(OH) C24:1 blood level 0.18, 95% CI 0.04 to 0.87, p = 0.033). Results were similar for 1-year mortality. Low admission sphingomyelin levels showed a weak association with poor neurological outcome in patients after cardiac arrest. If validated in future studies, a better understanding of biological sphingomyelin function during cardiac arrest may help to further advance the therapeutic approach and risk stratification in this vulnerable patient group.

Out-of-hospital cardiac arrest (OHCA) is a leading cause of mortality, yet the prediction of its outcome remains challenging. Serum Acyl Carnitines (ACs), a biomarker of beta-oxidation, have been associated with cardiovascular events. We evaluated the association of different AC species with mortality and neurological outcome in a cohort of OHCA patients.We consecutively included OHCA patients in this prospective observational study upon admission to the intensive care unit. We studied the association of thirty-nine different ACs measured at admission and 30-day mortality (primary endpoint), as well as neurological outcome at hospital discharge (secondary endpoint) using the Cerebral Performance Category scale. Multivariate models were adjusted for age, gender, comorbidities and shock markers.Of 281 included patients, 137 (48.8%) died within 30 days and of the 144 survivors (51.2%), 15 (10.4%) had poor neurological outcome. While several ACs were associated with mortality, AC C2 had the highest prognostic value for mortality (fully-adjusted odds ratio 4.85 (95%CI 1.8 to 13.06, p .01), area under curve (AUC) 0.65) and neurological outcome (fully-adjusted odds ratio 3.96 (95%CI 1.47 to 10.66, p .01), AUC 0.63).ACs are interesting surrogate biomarkers that are associated with mortality and poor neurological outcome in patients after OHCA and may help to improve the understanding of pathophysiological mechanisms and risk stratification.

Objectives:We determine the frequency, risk factors, and mortality of neurologic complications in adults on extracorporeal membrane oxygenation and propose an algorithm for preventive strategies.Data Sources:PubMed, Embase, and Cochrane databases.Study Selection:Screening was performed using predefi

Background: We investigated whether Neuron-specific enolase (NSE) serum concentration predicts long-term mortality and poor neurological outcome in adult cardiac arrest patients. Methods: Within this prospective observational study, we included consecutive adult patients admitted to the intensive care unit (ICU) after cardiac arrest. NSE was measured upon ICU admission and on days 1, 2, 3, 5 and 7. Results: Of 403 patients, 176 (43.7%) survived. Median follow-up duration was 43.7 months (IQR 14.3 to 63.0 months). NSE levels on day 3 were increased more than threefold in non-survivors compared to survivors (median NSE (ng/mL) 19.8 (IQR 15.7 to 27.8) vs. 72.6 (IQR 26 to 194)) and showed the highest prognostic performance for mortality compared to other days of measurement, with an AUC of 0.81 and an adjusted hazard ratio of 1.55 (95% CI 1.41 to 1.71, p &lt, 0.001). Subgroup analysis showed an excellent sensitivity and negative predictive value of 100% of NSE in patients &lt, 54 years of age. Conclusion: NSE measured three days after cardiac arrest is associated with long-term mortality and neurological outcome and may provide prognostic information that improves clinical decision making. Particularly in the subgroup of younger patients (&lt, 54 years), NSE showed excellent negative predictive value.

Objective:To determine the implications of first responses of emergency medical services (EMS) to out-of-hospital status epilepticus (SE) on outcome.Methods:From 2005 to 2014, prehospital and in-hospital data were assessed in consecutive adults admitted to an academic medical center with out-of-hospital SE. Logistic regression was performed to identify variables with a robust association between missed epileptic events by the EMS and no recovery to functional baseline in survivors.Results:Among 213 SE patients, 150 were admitted via EMS. While nonconvulsive SE (NCSE) was missed by the EMS in 63.7%, convulsive SE (CSE) was not missed except in 4 patients with transformation into subtle SE. Missed NCSE was more likely with older age (odds ratio [OR]per year 1.06, 95% confidence interval [CI] 1.02–1.10, p = 0.003) and no seizure history (OR 6.64, 95% CI 2.43–18.1, p < 0.001). The area under the receiver operating characteristic curve for prediction of missed NCSE by these variables was 0.839. Independent predictors for not receiving benzodiazepines were increasing age (ORper year 1.05, 95% CI 1.01–1.08, p = 0.008) and higher Glasgow Coma Scale score (ORper increasing unit 1.21, 95% CI 1.09–1.36, p = 0.001). Missed NCSE was independently associated with increased odds for no return to functional baseline in survivors (OR 3.83, 95% CI 1.22–11.98, p = 0.021).Conclusions:Among patients admitted with out-of-hospital SE, CSE is mostly recognized while NCSE is frequently missed especially in patients with increasing age and no seizure history. This calls for heightened awareness for out-of-hospital NCSE in such patients, as missed NCSE is associated with lack of treatment and less recovery to functional baseline in survivors independent of established outcome predictors.

Aim Neuron-specific enolase (NSE) increases in response to brain injury and is recommended for outcome prediction in cardiac arrest patients. Our aim was to investigate whether NSE measured at different days after a cardiac arrest and its kinetics would improve the prognostic ability of two cardiac arrest specific risk scores. Methods Within this prospective observational study, we included consecutive adult patients after cardiac arrest. We calculated the Out-of-hospital cardiac arrest (OHCA) score and the Cardiac Arrest Hospital Prognosis (CAHP) score upon ICU admission and measured serum NSE upon admission and days 1, 2, 3, 5 and 7. We calculated logistic regression models to study associations of scores and NSE levels with neurological outcome defined by Cerebral Performance Category (CPC) scale and in-hospital death. Results From 336 included patients, 180 (54%) survived until hospital discharge, of which 150 (45%) had a good neurological outcome. NSE at day 3 showed the highest prognostic accuracy (discrimination) for neurological outcome (area under the curve (AUC) 0.89) and in-hospital mortality (AUC 0.88). These results were robust in reclassification statistics and across different subgroups. NSE kinetics with admission levels serving as a baseline did not further improve prognostication. NSE on day 3 significantly improved discrimination of both clinical risk scores (CAHP from AUC 0.81 to 0.91; OHCA from AUC 0.79 to 0.89). Conclusion NSE measured at day 3 significantly improves clinical risk scores for outcome prediction in cardiac arrest patients and may thus add to clinical decision making about escalation or withdrawal of therapy in this vulnerable patient population.

Aim Several scores are available to predict mortality and neurological outcome in cardiac arrest patients admitted to the intensive care unit (ICU). The aim of the study was to externally validate the prognostic value of four previously published risk scores. Methods For this observational, single-center study, we prospectively included 349 consecutive adult cardiac arrest patients upon ICU admission. We calculated two cardiac arrest specific risk scores (OHCA and CAHP) and two general severity of illness scores (APACHE II and SAPS II). The primary endpoint was in-hospital mortality. Secondary endpoints were neurological outcome at hospital discharge and 30-day mortality. Results 170 patients (49%) died until hospital discharge. All scores were independently associated with outcomes in logistic regression analysis and showed acceptable discrimination for in-hospital mortality with highest AUCs of the cardiac arrest specific risk scores (OHCA: 0.80 (95%CI 0.75–0.85) and CAHP: 0.84 (95%CI 0.79–0.88) compared to the severity of illness scores (APACHE II: 0.78 (95%CI 0.73–0.83) and SAPS II: 0.77 (95%CI 0.72–0.82). Results were robust in subgroup analysis except for worse performance in elderly patients (>75 years) and patients with respiratory cause of cardiac arrest. Results were similar for 30-days mortality and slightly higher for neurological outcome. Conclusions This study confirms the good prognostic performance of cardiac arrest specific scores to predict mortality and neurological outcomes in cardiac arrest patients. Routine use of OHCA or CAHP score helps to objectively risk stratify these vulnerable patients and thereby may improve therapeutic decisions.

Prognostication of cardiac arrest patients admitted to the intensive care unit (ICU) may influence treatment decision, but remains challenging. We evaluated the incremental usefulness of routine blood markers from different biological pathways for predicting fatal outcome and neurological deficits in cardiac arrest patients.We prospectively included consecutive, adult cardiac arrest patients upon ICU admission. We recorded initial clinical parameters and measured blood markers of cardiac injury/stress (troponin, BNP, CK), inflammation/infection (WBC, CRP, procalcitonin) and shock (lactate, creatinine, urea). The primary and secondary endpoints were all-cause in-hospital mortality and bad neurological outcome defined by the Cerebral Performance Category (CPC) score.Mortality in the 321 included patients was 49% (n = 156). Procalcitonin (adjusted odds ratio 1.84, 95%CI 1.34 to 2.53, p 0.001; AUC 0.73) and lactate (adjusted odds ratio 7.29, 95%CI 3.05 to 17.42, p 0.001; AUC 0.70) were identified as independent prognostic factors for mortality and significantly improved discrimination of a parsimonious clinical model including resuscitation measures (no-flow time, shockable rhythm) and initial vital signs (Glasgow coma scale, respiratory rate) from an AUC of 0.79 to 0.84 (p 0.001). Cardiac markers did not further improve the model. Results for neurological outcome were similar with model improvements by procalcitonin and lactate from AUC 0.83 to 0.87 (p = 0.004).Assessment of routine markers of inflammation/infection and shock provide significant improvements for prognostication of cardiac arrest patients, while cardiac markers did not further improve statistical models. Combination of blood markers and clinical parameters may help to improve initial management decisions in this vulnerable patient population.

We present the case of a 63 year old man who died of severe septic shock in the setting of agranulocytosis induced by dipyrone (metamizole). The patient had previously developed agranulocytosis after dipyrone exposure 18 months prior to this. The case illustrates the seriousness of dipyrone-induced agranulocytosis, highlights the risks associated with re-exposure and underlines the need for excellent communication between treating physicians and their patients. The possible underlying mechanisms, epidemiology and management of dipyrone-induced agranulocytosis are discussed.

Background and purpose The aim was to determine differences of clinical, treatment and outcome characteristics between patients with in-hospital and out-of-hospital status epilepticus (SE). Methods From 2005 to 2014, clinical data were assessed in adults with SE treated in an academic medical care centre. Clinical characteristics, treatment and outcomes were compared between patients with in-hospital and out-of-hospital SE. Results Amongst 352 patients, 213 were admitted with SE and 139 developed in-hospital SE. Patients with in-hospital SE had more acute/fatal aetiologies (60% vs. 35%, P < 0.001), fewer previous seizures (33% vs. 50%, P = 0.002), a higher median Charlson Comorbidity Index (3 vs. 2, P < 0.001), longer median SE duration (1 vs. 0.5 days, P = 0.001), more refractory SE (52% vs. 39%, P = 0.022), less return to functional baseline (38% vs. 54%, P = 0.006) and increased mortality (29% vs. 19%, P = 0.001). Whilst in multivariable analyses an increasing Status Epilepticus Severity Score (STESS) was an independent predictor for death in both groups, increased Charlson Comorbidity Index and treatment refractory SE were associated with death only in patients with in-hospital SE. Continuous anaesthesia for refractory SE was associated with increased mortality only in patients with out-of-hospital SE. The area under the receiver operating curve was 0.717 for prediction of death by STESS in patients with in-hospital SE and 0.811 in patients with out-of-hospital SE. Conclusions Patients with in-hospital SE had more fatal aetiologies and comorbidities, refractory SE, less return to functional baseline, and increased mortality compared to patients with out-of-hospital SE. Whilst the STESS was a robust predictor for death in both groups, the association between continuous anaesthesia and death was limited to out-of-hospital SE.

We present the case of a 63 year old man who died of severe septic shock in the setting of agranulocytosis induced by dipyrone (metamizole). The patient had previously developed agranulocytosis after dipyrone exposure 18 months prior to this. The case illustrates the seriousness of dipyrone-induced agranulocytosis, highlights the risks associated with re-exposure and underlines the need for excellent communication between treating physicians and their patients. The possible underlying mechanisms, epidemiology and management of dipyrone-induced agranulocytosis are discussed.Wir stellen den Fall eines 63-jährigen Mannes vor, der einen schweren septischen Schock mit letalem Ausgang auf Basis einer Agranulozytose entwickelte. Aufgrund des zeitlichen Zusammenhangs, der Verbesserung nach Dechallenge in der Vorgeschichte und aktuellem Rechallenge ist der Kausalzusammenhang für eine erneute Metamizol-induzierte Agranulozytose sicher. Wir diskutieren die Wichtigkeit, Patienten mit einer verdächtigten Metamizol-induzierten Agranulozytose nicht erneut zu exponieren und Patienten sowie behandelnde Ärzte lückenlos zu informieren.