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Objectives: Hyperoxia could lead to a worse outcome after cardiac arrest. Few studies have investigated the impact of oxygenation status on patient outcomes following extracorporeal cardiopulmonary resuscitation. We sought to delineate the association between oxygenation status and neurologic outcomes in patients receiving extracorporeal cardiopulmonary resuscitation. Design: Retrospective analysis of a prospective extracorporeal cardiopulmonary resuscitation registry database. Setting: An academic tertiary care hospital. Patients: Patients receiving extracorporeal cardiopulmonary resuscitation between 2000 and 2014. Interventions: None. Measurements and Main Results: A total of 291 patients were included, and 80.1% were male. Their mean age was 56.0 years. The arterial blood gas data employed in the primary analysis were recorded from the first sample over the first 24 hours in the ICUs after return of spontaneous circulation. The mean Pao 2 after initiation of venoarterial extracorporeal membrane oxygenation was 178.0 mm Hg, and the mean Pao 2/Fio 2 ratio was 322.0. Only 88 patients (30.2%) demonstrated favorable neurologic status at hospital discharge. Multivariate logistic regression analysis indicated that Pao 2 between 77 and 220 mm Hg (odds ratio, 2.29; 95% CI, 1.01–5.22; p = 0.05) and Pao 2/Fio 2 ratio between 314 and 788 (odds ratio, 5.09; 95% CI, 2.13–12.14; p < 0.001) were both positively associated with favorable neurologic outcomes. Conclusions: Oxygenation status during extracorporeal membrane oxygenation affects neurologic outcomes in patients receiving extracorporeal cardiopulmonary resuscitation. The Pao 2 range of 77 to 220 mm Hg, which is slightly narrower than previously defined, seems optimal. The Pao 2/Fio 2 ratio was also associated with outcomes in our analysis, indicating that both Pao 2 and the Pao 2/Fio 2 ratio should be closely monitored during the early postcardiac arrest phase for postextracorporeal cardiopulmonary resuscitation patients.

Urinary biomarkers augment the diagnosis of acute kidney injury (AKI), with AKI after cardiovascular surgeries being a prototype of prognosis scenario. Glutathione S-transferases (GST) were evaluated as biomarkers of AKI. Urine samples were collected in 141 cardiovascular surgical patients and analyzed for urinary alpha-(α-) and pi-(π-) GSTs. The outcomes of advanced AKI (KDIGO stage 2, 3) and allcause in-patient mortality, as composite outcome, were recorded. Areas under the receiver operator characteristic (ROC) curves and multivariate generalized additive model (GAM) were applied to predict outcomes. Thirty-eight (26.9%) patients had AKI, while 12 (8.5%) were with advanced AKI. Urinary π-GST differentiated patients with/without advanced AKI or composite outcome after surgery (p < 0.05 by generalized estimating equation). Urinary π-GST predicted advanced AKI at 3 hrs post-surgery (p = 0.033) and composite outcome (p = 0.009), while the corresponding ROC curve had AUC of 0.784 and 0.783. Using GAM, the cutoff value of 14.7 μg/L for π-GST showed the best performance to predict composite outcome. The addition of π-GST to the SOFA score improved risk stratification (total net reclassification index = 0.47). Thus, urinary π-GST levels predict advanced AKI or hospital mortality after cardiovascular surgery and improve in SOFA outcome assessment specific to AKI.In a physician's daily clinical practice, the evaluation of kidney function is certainly part of the comprehensive care for patients, with collection of numerous data points for association of acute kidney injury (AKI) and adverse clinical outcome 1 . Creatinine is certainly a useful tool for evaluation of kidney excretory function. However, it tells little about whether structural damage coexists or precedes the functional change. Urinary biomarkers have been proposed to predict and/or augment the diagnosis of AKI in order to overcome the limitations inherent to creatinine and urine output criteria, i.e., inadequate sensitivity and delayed response. A variety of serum and urinary biomarkers have been under extensive investigation and validation 2 since the pioneer study series of neutrophil gelatinase-associated lipocalin (NGAL) more than a decade ago 3,4 . Biomarkers of AKI could be used to evaluate the severity of AKI at an earlier time point in the course of the disease, defining those with high risk of progression to more advanced kidney injury. Moreover, there is urgent need to use novel biomarkers as a guide for clinical decision-making, and augmenting selection of effective management strategies for advanced AKI, e.g. dialysis. The list of candidate biomarkers is ever-growing 5 , including but not limited to neutrophil gelatinase-associated lipocalin (NGAL), liver fatty acid-binding protein (L-FABP), kidney injury molecule 1 (KIM1), interleukin-18 (IL-18), cystatin C, and the combination of tissue inhibitor of metalloproteinase-2 (TIMP-2) and insulin-like growth factor binding protein 7 (IGFBP7), either serum or urine concentration. However, the predic...

BackgroundMicrocirculatory dysfunction develops in both septic and cardiogenic shock patients, and it is associated with poor prognosis in patients with septic shock. Information on the association between microcirculatory dysfunction and prognosis in cardiogenic shock patients with venoarterial extracorporeal membrane oxygenation (VA-ECMO) support is limited.MethodsSublingual microcirculation images were recorded using an incident dark-field video microscope at the following time points: within 12 h (T1), 24 h (T2), 48 h (T3), 72 h (T4), and 96 h (T5) after VA-ECMO placement. If a patient could be weaned off VA-ECMO, sublingual microcirculation images were recorded before and after VA-ECMO removal. Microcirculatory parameters were compared between 28-day nonsurvivors and survivors with VA-ECMO support. In addition, the microcirculation and clinical parameters were assessed as prognostic tests of 28-day mortality, and patients were divided into three subgroups according to microcirculation parameters for survival analysis.ResultsForty-eight patients were enrolled in this study. At T1, the observed heart rate, mean arterial pressure, inotropic score and lactate level of 28-day nonsurvivors and survivors did not differ significantly, but the perfused small vessel density (PSVD) and proportion of perfused vessels (PPV) were lower in the 28-day nonsurvivors than in the survivors. The PSVD and PPV were slightly superior to lactate levels in predicting 28-day mortality (area under curve of 0.68, 0.70, and 0.62, respectively). The subgroup with the lowest PSVD (< 15 mm/mm2) and PPV (< 64%) values exhibited less favorable survival compared with the other two subgroups.ConclusionsEarly microcirculatory parameters could be used to predict the survival of cardiogenic shock patients with VA-ECMO support.Trial registrationClinicalTrials.gov, NCT02393274. Registered on 19 March 2015.

Acute kidney injury (AKI) is detrimental after cardiac surgery. In this multicenter study, the novel biomarker hemojuvelin (HJV) was evaluated for AKI prediction following cardiac surgery. Urinary HJV, neutrophil gelatinase-associated lipocalin (NGAL), and urinary creatinine were measured in 151 patients after surgery. The outcomes of advanced AKI (KDIGO stages 2 and 3) and all causes of in-hospital mortality as the composite outcome were recorded. Areas under the receiver operator characteristic curves (AUC) and a multivariate generalized additive model (GAM) were applied to predict these outcomes of interest. Urinary HJV differentiated patients with/without AKI, advanced AKI or composite outcome after surgery (p < 0.001, by a generalized estimating equation) in this study. At three hours post-surgery, urinary HJV predicted advanced AKI (p < 0.001) and composite outcome (p < 0.001) with corresponding AUC values of 0.768 and 0.828, respectively. The performance of creatinine-adjusted HJV was also superior to NGAL in predicting advanced AKI (AUC = 0.784 and 0.694; p = 0.037) and composite outcome (AUC = 0.842 and 0.676; p = 0.002). The integration of HJV into the Cleveland Clinic score for advanced AKI led to a significant increase in risk stratification (net reclassification improvement [NRI] = 0.598; p < 0.001).