• disseminated intravascular coagulation
• in-hospital cardiac arrest
• prognosis
• scoring
• targeted temperature management

• Biomarkers
• Cardiac arrest
• Cardiopulmonary resuscitation
• Extracorporeal membrane oxygenation

• Humans
• Male
• Female
• Out-of-Hospital Cardiac Arrest/therapy
• Out-of-Hospital Cardiac Arrest/blood
• Out-of-Hospital Cardiac Arrest/mortality
• Biomarkers/blood
• Cardiopulmonary Resuscitation/methods
• Middle Aged
• Extracorporeal Membrane Oxygenation/methods
• Prognosis
• Aged
• Procalcitonin/blood
• Phosphopyruvate Hydratase/blood

• Cardiac arrest
• Cardiopulmonary resuscitation
• In-hospital cardiac arrest
• Myocardial dysfunction
• Out-of-hospital cardiac arrest
• Post-resuscitation
• Stony heart

• MIMIC-IV database
• all-cause mortality
• cardiac arrest
• critical care
• international normalized ratio

• Humans
• Treatment Outcome
• Prospective Studies
• Cardiopulmonary Resuscitation
• Blood Coagulation
• Out-of-Hospital Cardiac Arrest
• Lactic Acid

• ZOLL Foundation

• critical care
• endothelium
• glycocalyx
• hemostasis
• precision medicine
• resuscitation
• shock
• thromboelastography

To estimate the incidence, risk factors, and impact on mortality and functional outcomes for early coagulopathy after the return of spontaneous circulation (ROSC) in pediatric out-of-hospital cardiac arrest (OHCA) patients.

A post hoc analysis of the Therapeutic Hypothermia after Pediatric Cardiac Arrest Out-of-Hospital (THAPCA-OH) trial was conducted. Early coagulopathy was defined as presence of at least one of the following coagulation abnormalities upon admission: international standard ratio (INR), platelets, and age-adjusted activated partial thromboplastin time (APTT) within 6 h after OHCA and before therapeutic hypothermia initiation. The outcomes included 28-day mortality and functional prognosis. Multivariable logistic regression models were used to explore risk factors and association between early coagulopathy and outcomes.

Of the 227 patients included, 152 (67%) were male and the median age was 2.3 years [interquartile range (IQR), 0.7–8.6 years]. The overall 28-day mortality was 63%. The incidence of early coagulopathy was 46%. Lower age, longer duration of chest compression, lower temperature, and higher white blood cell (WBC) upon admission increased the risk of early coagulopathy. Early coagulopathy [OR, 2.20 (95% CI, 1.12–4.39), P = 0.023] was independently associated with 28-day mortality after adjusting for confounders.

Early coagulopathy occurred in almost half of pediatric patients with OHCA. Lower age, longer duration of chest compression, lower temperature, and higher WBC increased the risk. The development of early coagulopathy was independently associated with increased mortality.

The online version contains supplementary material available at 10.1186/s12959-022-00422-x.

• Children
• Coagulopathy
• Out-of-hospital cardiac arrest
• Prognosis

• Cardiac arrest
• Intensive care medicine
• Kynurenine
• Post-cardiac arrest syndrome
• Prognostication
• Tryptophan

In recent years, gamma-glutamyl transpeptidase to platelet ratio (GPR) has been proposed as a new inflammatory marker. We aimed to evaluate the association between GPR and outcomes after cardiac arrest (CA).

A total of 354 consecutive patients with CA were included in this retrospective study. Patients were divided into three groups according to tertiles of GPR (low, n = 119; middle, n = 117; and high, n = 118). To determine the relationship between GPR and prognosis, a logistic regression analysis was performed. The ability of GPR to predict the outcomes was evaluated by receiver operating characteristic (ROC) curve analysis. Two prediction models were established, and the likelihood ratio test (LRT) and the Akaike Information Criterion (AIC) were utilized for model comparison.

Among the 354 patients (age 62 [52, 74], 254/354 male) who were finally included in the analysis, those in the high GPR group had poor outcomes. Multivariate logistic regression analysis revealed that GPR was independently associated with the three outcomes, for ICU mortality (odds ratios (OR) = 1.738, 95% confidence interval (CI): 1.221-2.474, P = 0.002), hospital mortality (OR = 1.676[1.164 − 2.413], P = 0.005), and unfavorable neurologic outcomes (OR = 1.623[1.121 − 2.351], P = 0.010). The area under the ROC curve was 0.611 (95% Cl: 0.558-0.662) for ICU mortality, 0.600 (95% CI: 0.547-0.651) for hospital mortality, and 0.602 (95% CI: 0.549-0.653) for unfavorable neurologic outcomes. Further, the LRT analysis showed that compared with the model without GPR, the GPR-combined model had a higher likelihood ratio χ² score and smaller AIC.

GPR, as an inflammatory indicator, was independently associated with outcomes after CA. GPR is helpful in estimating the clinical outcomes of patients with CA.

• Coagulation activation
• Factor IXa-antithrombin complex
• Factor XIa-antithrombin complex
• Out-of-hospital cardiac arrest
• Prognosis
• Thrombin-antithrombin complex

• disseminated intravascular coagulation
• haemorrhage
• neoplasms
• sepsis
• thrombosis

• Cardiac arrest
• disseminated intravascular coagulation score (DIC score)
• neuron-specific enolase (NSE)

• Cardiac arrest
• Neurologic progronsis
• Postcardiac arrest syndrome
• Targeted temperature management
• Thromboleastography

• arrhythmogenic right ventricular cardiomyopathy
• epsilon waves
• extracorporeal life support
• sudden cardiac death

• K23 HL141596 NHLBI NIH HHS
• National Heart, Lung, and Blood Institute
• National Institutes of Health

• Chronic kidney disease
• Out-of-hospital cardiac arrest
• Targeted temperature management

• Aged
• Cardiopulmonary Resuscitation/statistics & numerical data
• Case-Control Studies
• Female
• Humans
• Hypothermia, Induced/adverse effects
• Hypothermia, Induced/statistics & numerical data
• Kidney Failure, Chronic/epidemiology
• Male
• Middle Aged
• Out-of-Hospital Cardiac Arrest/mortality
• Out-of-Hospital Cardiac Arrest/therapy
• Registries
• Retrospective Studies

Supplemental Digital Content is available in the text.

Recent data suggest that early increased fibrinolysis may be associated with unfavorable prognosis in cardiac arrest. The current study aimed to assess whether there is an optimal fibrinolysis cutoff value as determined by thrombelastometry at hospital admission to predict poor outcome in a cohort of adult patients with out-of-hospital cardiac arrest.

Prospective observational cohort study.

Emergency department of a 2.100-bed tertiary care facility in Vienna, Austria, Europe.

Patients with out-of-hospital cardiac arrest of presumed cardiac origin, subjected to targeted temperature management, who had achieved return of spontaneous circulation at admission were analyzed.

None.

Fibrinolysis was assessed by thrombelastometry at the bedside immediately after hospital admission and is given as maximum lysis (%). The outcome measure was the optimal cutoff for maximum lysis at hospital admission to predict poor outcome (a composite of Cerebral Performance Category 3–5 or death) at day 30, assessed by receiver operating characteristic curve analysis. Seventy-eight patients (61% male, median 59 yr) were included in the study from March 2014 to March 2017. Forty-two patients (54%) had a poor 30-day outcome including 23 nonsurvivors (30%). The maximum lysis cutoff at admission predicting poor 30-day outcome with 100% specificity (95% CI, 90–100%) was greater than or equal to 20%. Tissue-type plasminogen activator antigen levels were likewise elevated in patients with poor neurologic outcome or death 52 ng/mL (interquartile range, 26–79 ng/mL) versus 29 ng/mL (interquartile range, 17–49 ng/mL; p = 0.036).

Increased fibrinolysis at admission assessed by thrombelastometry specifically predicts poor outcome in cardiac arrest with presumed cardiac etiology.

• cardiac arrest
• disseminated intravascular coagulation
• fibrinolysis
• inflammation
• resuscitation

• Animals
• Blood Coagulation
• Disseminated Intravascular Coagulation/blood
• Disseminated Intravascular Coagulation/etiology
• Disseminated Intravascular Coagulation/mortality
• Disseminated Intravascular Coagulation/therapy
• Fibrinolysis
• Heart Arrest/blood
• Heart Arrest/complications
• Heart Arrest/mortality
• Heart Arrest/therapy
• Humans
• Multiple Organ Failure/blood
• Multiple Organ Failure/etiology
• Multiple Organ Failure/mortality
• Resuscitation/adverse effects
• Resuscitation/mortality
• Risk Factors
• Treatment Outcome

• cardiac arrest
• coagulation
• disseminated intravascular coagulation
• extracorporeal cardiopulmonary resuscitation
• extracorporeal membrane oxygenation
• refractory cardiac arrest

• Disseminated intravascular coagulation
• Fibrinolysis
• Out-of-hospital cardiac arrest
• Prognostic factors
• Resuscitation

• Aged
• Austria/epidemiology
• Disseminated Intravascular Coagulation/mortality
• Female
• Fibrin Fibrinogen Degradation Products/analysis
• Fibrinolysis
• Humans
• Kaplan-Meier Estimate
• Logistic Models
• Male
• Middle Aged
• Out-of-Hospital Cardiac Arrest/mortality
• Out-of-Hospital Cardiac Arrest/therapy
• Prognosis
• Prospective Studies
• ROC Curve
• Resuscitation
• Severity of Illness Index
• Time Factors

• criteria
• disseminated intravascular coagulation
• mortality
• scoring
• trauma

• Aged
• Area Under Curve
• Disseminated Intravascular Coagulation/mortality
• Female
• Fibrinogen/analysis
• Humans
• Male
• Middle Aged
• Odds Ratio
• Predictive Value of Tests
• Prognosis
• Retrospective Studies
• Trauma Severity Indices
• Wounds and Injuries/mortality

• activation of coagulation
• disseminated intravascular coagulation
• fibrinolytic shutdown
• impaired anticoagulant
• no-reflow phenomenon
• post-cardiac arrest syndrome
• systemic ischemia/reperfusion

• Coagulation
• Haemostasis
• Heart arrest
• Hypothermia
• Targeted temperature management

One quarter of patients suffering from acute critical illness such as severe trauma, sepsis, myocardial infarction (MI) or post cardiac arrest syndrome (PCAS) develop severe hemostatic aberrations and coagulopathy, which are associated with excess mortality. Despite the different types of injurious “hit”, acutely critically ill patients share several phenotypic features that may be driven by the shock. This response, mounted by the body to various life-threatening conditions, is relatively homogenous and most likely evolutionarily adapted. We propose that shock-induced sympatho-adrenal hyperactivation is a critical driver of endothelial cell and glycocalyx damage (endotheliopathy) in acute critical illness, with the overall aim of ensuring organ perfusion through an injured microvasculature. We have investigated more than 3000 patients suffering from different types of acute critical illness (severe trauma, sepsis, MI and PCAS) and have found a potential unifying pathologic link between sympatho-adrenal hyperactivation, endotheliopathy, and poor outcome. We entitled this proposed disease entity, shock-induced endotheliopathy (SHINE). Here we review the literature and discuss the pathophysiology of SHINE.

• biological marker
• heart arrest
• mean platelet volume
• mortality
• patient outcome assessment

• Adult
• Aged
• Biomarkers/blood
• Endothelium, Vascular/pathology
• Female
• Hospital Mortality
• Humans
• Inflammation
• Male
• Mean Platelet Volume
• Middle Aged
• Out-of-Hospital Cardiac Arrest/blood
• Out-of-Hospital Cardiac Arrest/mortality
• Patient Admission
• Platelet Activation
• Proportional Hazards Models
• Reperfusion Injury
• Resuscitation
• Retrospective Studies
• Sepsis/pathology
• Time Factors
• Treatment Outcome

We tested the hypothesis that disseminated intravascular coagulation (DIC) during the early phase of post-cardiopulmonary resuscitation (CPR) is associated with systemic inflammatory response syndrome (SIRS), multiple organ dysfunction syndrome (MODS) and affects the outcome of out-of-hospital cardiac arrest (OHCA) patients.

A review of the computer-based medical records of OHCA patients was retrospectively conducted and included 388 patients who were divided into DIC and non-DIC patients based on the Japanese Association for Acute Medicine DIC diagnostic criteria. DIC patients were subdivided into two groups: those with and without hyperfibrinolysis. Pre-hospital factors, platelet count, coagulation and fibrinolysis markers and lactate levels within 24 h after resuscitation were evaluated. The outcome measure was all-cause hospital mortality.

DIC patients exhibited lower platelet counts, prolonged prothrombin time, decreased levels of fibrinogen and antithrombin associated with increased fibrinolysis than those without DIC. DIC patients more frequently developed SIRS and MODS, followed by worse outcomes than non-DIC patients. The same changes were observed in DIC patients with hyperfibrinolysis who showed a higher prevalence of MODS, leading to worse outcome than those without hyperfibrinolysis. Logistic regression analyses showed that lactate levels predicted hyperfibrinolysis and DIC is an independent predictor of patient death. Survival probabilities of DIC patients during hospital stay were significantly lower than non-DIC patients. The area under the receiver operating characteristic curve of DIC for the prediction of death was 0.704.

The fibrinolytic phenotype of DIC during the early phase of post-CPR more frequently results in SIRS and MODS, especially in patients with hyperfibrinolysis, and affects the outcome of OHCA patients.

The online version of this article (doi:10.1186/s12959-016-0116-y) contains supplementary material, which is available to authorized users.

• Cardiac arrest
• Disseminated intravascular coagulation (DIC)
• Fibrinolysis
• Out-of-hospital
• Outcome

• Advanced cardiac life support
• Cardiopulmonary resuscitation
• Cerebral ischaemia
• Prognosis

• Aged
• Cardiopulmonary Resuscitation
• Female
• Forecasting
• Humans
• Male
• Out-of-Hospital Cardiac Arrest/mortality
• Out-of-Hospital Cardiac Arrest/therapy
• Regression Analysis
• Treatment Outcome

Pulmonary edema is frequently observed after a successful resuscitation in out-of-hospital cardiac arrest (OHCA) patients. Currently, its risk factors and prognostic implications are mostly unknown.

Adult OHCA patients with a presumed cardiac etiology who achieved sustained return of spontaneous circulation (ROSC) in emergency department were retrospectively analyzed. The patients were grouped according to the severity of consolidation on their initial chest X-ray (group I, no consolidation; group II, patchy consolidations; group III, consolidation involving an entire lobe; group IV, total white-out of any lung). The primary objective was to identify the risk factors of developing severe pulmonary edema (group III or IV). The secondary objective was to evaluate the association between long-term prognosis and the severity of pulmonary edema.

One hundred and seven patients were included. Total duration of cardiopulmonary resuscitation (CPR) and initial pCO₂ level were both independent predictors of developing severe pulmonary edema with their odds ratio (OR) being 1.02 (95% confidence interval [CI], 1.00 to 1.04; per 1 minute) and 1.04 (95% CI, 1.01 to 1.07; per 1 mmHg), respectively. The long term prognosis was significantly poor in patients with severe pulmonary edema with a OR for good outcome (6-month cerebral performance category 1 or 2) being 0.22 (95% CI, 0.06 to 0.79) in group III and 0.16 (95% CI, 0.04 to 0.63) in group IV compared to group I.

The duration of CPR and initial pCO₂ level were both independent predictors for the development of severe pulmonary edema after resuscitation in emergency department. The severity of the pulmonary edema was significantly associated with long-term outcome.

• Cardiopulmonary resuscitation
• Prognosis
• Pulmonary edema
• Ventilation

Patients with severe sepsis often present with concurrent coagulopathy, microcirculatory failure and evidence of vascular endothelial activation and damage. Given the critical role of the endothelium in balancing hemostasis, we investigated single-point associations between whole blood coagulopathy by thrombelastography (TEG) and plasma/serum markers of endothelial activation and damage in patients with severe sepsis.

A post-hoc multicenter prospective observational study in a subgroup of 184 patients from the Scandinavian Starch for Severe Sepsis/Septic Shock (6S) Trial. Study patients were admitted to two Danish intensive care units. Inclusion criteria were severe sepsis, pre-intervention whole blood TEG measurement and a plasma/serum research sample available from baseline (pre-intervention) for analysis of endothelial-derived biomarkers. Endothelial-derived biomarkers were measured in plasma/serum by enzyme-linked immunosorbent assay (syndecan-1, thrombomodulin, protein C (PC), tissue-type plasminogen activator and plasminogen activator inhibitor-1). Pre-intervention TEG, functional fibrinogen (FF) and laboratory and clinical data, including mortality, were retrieved from the trial database.

Most patients presented with septic shock (86%) and pulmonary (60%) or abdominal (30%) focus of infection. The median (IQR) age was 67 years (59 to 75), and 55% were males. The median SOFA and SAPS II scores were 8 (6 to 10) and 56 (41 to 68), respectively, with 7-, 28- and 90-day mortality rates being 21%, 39% and 53%, respectively. Pre-intervention (before treatment with different fluids), TEG reaction (R)-time, angle and maximum amplitude (MA) and FF MA all correlated with syndecan-1, thrombomodulin and PC levels. By multivariate linear regression analyses, higher syndecan-1 and lower PC were independently associated with TEG and FF hypocoagulability at the same time-point: 100 ng/ml higher syndecan-1 predicted 0.64 minutes higher R-time (SE 0.25), 1.78 mm lower TEG MA (SE 0.87) and 0.84 mm lower FF MA (SE 0.42; all P <0.05), and 10% lower protein C predicted 1.24 mm lower TEG MA (SE 0.31).

In our cohort of patients with severe sepsis, higher circulating levels of biomarkers of mainly endothelial damage were independently associated with hypocoagulability assessed by TEG and FF. Endothelial damage is intimately linked to coagulopathy in severe sepsis.

Clinicaltrials.gov number: NCT00962156. Registered 13 July 2009.

We studied associations of the stress hormones copeptin and cortisol with outcome and organ dysfunction after out-of-hospital cardiac arrest (OHCA).

Plasma was obtained after consent from next of kin in the FINNRESUSCI study conducted in 21 Finnish intensive care units (ICUs) between 2010 and 2011. We measured plasma copeptin (pmol/L) and free cortisol (nmol/L) on ICU admission (245 patients) and at 48 hours (additional 33 patients). Organ dysfunction was categorised with 24-hour Sequential Organ Failure Assessment (SOFA) scores. Twelve-month neurological outcome (available in 276 patients) was classified with cerebral performance categories (CPC) and dichotomised into good (CPC 1 or 2) or poor (CPC 3 to 5). Data are presented as medians and interquartile ranges (IQRs). A Mann–Whitney U test, multiple linear and logistic regression tests with odds ratios (ORs) 95% confidence intervals (CIs) and beta (B) values, repeated measure analysis of variance, and receiver operating characteristic curves with area under the curve (AUC) were performed.

Patients with a poor 12-month outcome had higher levels of admission copeptin (89, IQR 41 to 193 versus 51, IQR 29 to 111 pmol/L, P = 0.0014) and cortisol (728, IQR 522 to 1,017 versus 576, IQR 355 to 850 nmol/L, P = 0.0013). Copeptin levels fell between admission and 48 hours (P <0.001), independently of outcome (P = 0.847). Cortisol levels did not change between admission and 48 hours (P = 0.313), independently of outcome (P = 0.221). The AUC for predicting long-term outcome was weak for copeptin (0.62, 95% CI 0.55 to 0.69) and cortisol (0.62, 95% CI 0.54 to 0.69). With logistic regression, admission copeptin (standard deviation (SD) increase OR 1.4, 95% CI 1.03 to 1.98) and cortisol (SD increase OR 1.5, 95% CI 1.1 to 2.0) predicted ICU mortality but not 12-month outcome. Admission factors correlating with SOFA were shockable rhythm (B −1.3, 95% CI −2.2 to −0.5), adrenaline use (B 1.1, 95% CI 0.2 to 2.0), therapeutic hypothermia (B 1.3 95% CI 0.4-2.2), and copeptin (B 0.04, 95% CI 0.02 to 0.07).

Admission copeptin and free cortisol were not of prognostic value regarding 12-month neurological outcome after OHCA. Higher admission copeptin and cortisol were associated with ICU death, and copeptin predicted subsequent organ dysfunction.

The online version of this article (doi:10.1186/s13054-015-0831-y) contains supplementary material, which is available to authorized users.

The post-resuscitation phase after out-of-hospital cardiac arrest (OHCA) is characterised by a systemic inflammatory response (e.g., severe sepsis), for which the immature granulocyte count is a diagnostic marker. In this study we evaluated the prognostic significance of the delta neutrophil index (DNI), which is the difference in leukocyte subfractions as assessed by an automated blood cell analyser, for early mortality after OHCA.

OHCA records from the emergency department cardiac arrest registry were retrospectively analysed. Patients who survived at least 24 h after return of spontaneous circulation were included in the analysis. We evaluated mortality and cerebral performance category scores at 30 days.

A total of 83 patients with OHCA were included in the study. Our results showed that DNI >8.4% on day 1 (hazard ratio [HR], 3.227; 95% CI, 1.485–6.967; p = 0.001) and DNI >10.5% on day 2 (HR, 3.292; 95% CI, 1.662–6.519; p<0.001) were associated with increased 30-day mortality in patients with OHCA. Additionally, DNI >8.4% on day 1 (HR, 2.718; 95% CI, 1.508–4.899; p<0.001) and DNI >10.5% on day 2 (HR, 1.709; 95% CI, 1.051–2.778; p = 0.02) were associated with worse neurologic outcomes 30 days after OHCA.

A higher DNI is a promising prognostic marker for 30-day mortality and neurologic outcomes after OHCA. Our findings indicate that patients with elevated DNI values after OHCA might be closely monitored so that appropriate treatment strategies can be implemented.

• Aged
• Biomarkers/blood
• Cardiopulmonary Resuscitation
• Female
• Humans
• Kaplan-Meier Estimate
• Male
• Middle Aged
• Neutrophils/cytology
• Out-of-Hospital Cardiac Arrest/blood
• Out-of-Hospital Cardiac Arrest/diagnosis
• Out-of-Hospital Cardiac Arrest/therapy
• Prognosis
• Retrospective Studies

Out-of-hospital cardiac arrest (OHCA) patients unresponsive to basic life support are frequently transferred to emergency departments (EDs) for further resuscitation. Although some survive with good neurologic outcomes, additional resuscitation in EDs is often futile. Without a dedicated termination of resuscitation (TOR) rule for ED resuscitation, the decision when to stop the resuscitation is up to emergency physicians. In this study, we assessed the association between patient characteristics and duration of resuscitation in EDs to understand how emergency physicians decide when to terminate cardiopulmonary resuscitation.

A retrospective analysis of the OHCA registry of a single ED was conducted. Adult (18 years or older) patients without any return of spontaneous circulation (ROSC) after unsuccessful ED advanced cardiac life support were included. The primary endpoint was duration of resuscitation attempts. Prehospital and demographic factors were assessed as independent variables. The relationship between these factors and duration of resuscitative attempts was analyzed with multivariable quantile regression.

From January 2008 to August 2012, ED resuscitation was terminated without ROSC in 266 patients (53.5%). The duration of resuscitative attempts was significantly shorter if any of the currently recognized poor prognostic factors was present. Interestingly, controversial factors such as female sex and older age were significantly associated with shorter resuscitation duration, while factors definitively indicating poor prognosis, such as severe trauma and poor baseline neurological status, showed no significant association.

The results of this study suggest that physicians adjust the resuscitation duration according to their subjective prediction of futility despite the absence of evidence-based TOR guidelines.

• Cardiac arrest
• Ethics
• Resuscitation

The kynurenine pathway (KP) is the major route of tryptophan (TRP) catabolism and is activated by inflammation and after cardiac arrest in animals. We hypothesized that the KP activation level correlates with severity of post–cardiac arrest shock, early death, and long‐term outcome.

Plasma was obtained from 245 patients enrolled in a prospective multicenter observational study in 21 intensive care units in Finland. Time to return of spontaneous circulation, lowest systolic arterial pressure, and bicarbonate during the first 24 hours were collected. A cerebral performance category of 3 to 5 defined 12‐month poor outcome. Plasma TRP and KP metabolites, kynurenine (KYN), kynurenic acid, 3‐hydroxyanthranilic acid, and the ratio of KYN to TRP were measured by liquid chromatography and mass spectrometry. All KP metabolites at intensive care unit admission were significantly higher in cardiac arrest patients with a nonshockable rhythm compared to those with a shockable rhythm, and kynurenic acid and 3‐hydroxyanthranilic acid correlated with time to return of spontaneous circulation. Patients with higher levels of KYN, KYN to TRP, kynurenic acid, and 3‐hydroxyanthranilic acid had lower 24‐hour systolic arterial pressure and bicarbonate. All KP metabolites and the ratio of KYN to TRP, but not TRP, were significantly higher in patients who died in the intensive care unit in comparison to those who survived. Multivariable logistic regression showed that high kynurenic acid (odds ratio: 1.004; 95% confidence interval: 1.001 to 1.008; P=0.014), and 3‐hydroxyanthranilic acid (odds ratio: 1.011; 95% confidence interval: 1.001 to 1.022; P=0.03) were independently associated with 12‐month poor outcome and significantly improved risk reclassification.

KP is activated early after cardiac arrest and is associated with severity of post–cardiac arrest shock, early death, and poor long‐term outcome.

• brain
• cardiac arrest
• kynurenine
• shock
• survival
• tryptophan

• Avalanche
• Burial
• Cardiac arrest
• Hypothermia

• adverse events
• cardiac arrest
• outcome
• predictors
• prognosis
• therapeutic hypothermia