Background: The prevalence of extracorporeal cardiopulmonary resuscitation (ECPR) in patients with out-of-hospital cardiac arrest (OHCA) has been increasing rapidly worldwide. However, guidelines or clinical studies do not provide sufficient data on ECPR practice. The aim of this study was to provide real-world data on ECPR for patients with OHCA, including details of complications.Methods: We did a retrospective database analysis of observational multicenter cohort study in Japan. Adult patients with OHCA of presumed cardiac etiology who received ECPR between 2013 and 2018 were included. The primary outcome was favorable neurological outcome at hospital discharge, defined as a cerebral performance category of 1 or 2.Results: A total of 1644 patients with OHCA were included in this study. The patient age was 18–93 years (median: 60 years). Shockable rhythm in the initial cardiac rhythm at the scene was 69.4%. The median estimated low flow time was 55 min (interquartile range: 45–66 min). Favorable neurological outcome at hospital discharge was observed in 14.1% of patients, and the rate of survival to hospital discharge was 27.2%. The proportions of favorable neurological outcome at hospital discharge in terms of shockable rhythm, pulseless electrical activity, and asystole were 16.7%, 9.2%, and 3.9%, respectively. Complications were observed during ECPR in 32.7% of patients, and the most common complication was bleeding, with the rates of cannulation site bleeding and other types of hemorrhage at 16.4% and 8.5%, respectively.Conclusions: In this large cohort, data on the ECPR of 1644 patients with OHCA show that the proportion of favorable neurological outcomes at hospital discharge was 14.1%, survival rate at hospital discharge was 27.2%, and complications were observed during ECPR in 32.7%.

Aneurysmal subarachnoid hemorrhage is a life-threatening disease requiring neurocritical care. Delayed cerebral ischemia is a well-known complication that contributes to unfavorable neurological outcomes. Cerebral vasospasm has been thought to be the main cause of delayed cerebral ischemia, and although several studies were able to decrease cerebral vasospasm, none showed improved neurological outcomes. Our target is not cerebral vasospasm but improving neurological outcomes. The purpose of this review is to discuss what intensivists should know and can do to improve clinical outcomes in subarachnoid hemorrhage patients. Delayed cerebral ischemia is thought to be due to not only vasospasm but also multifactorial mechanisms. Additionally, the concept of early brain injury, which occurs within the first 72 h after the hemorrhage, has become an important concern. Increasing sympathetic activity after the hemorrhage is associated with cardiopulmonary complications and poor outcomes. Serum lactate measurement may be a valuable marker reflecting the severity of sympathetic activity. The transpulmonary thermodilution method will bring about an advanced understanding of hemodynamic management. Fever is a well-recognized symptom and targeted temperature management is an anticipated intervention. To avoid hyperglycemia and hypoglycemia, performing moderate glucose control and minimizing glucose variability are important concepts in glycemic management, but the optimal target range remains unknown. Dysnatremia seems to be associated with negative outcomes. It is not clear yet that maintaining normonatremia actively improves neurological outcomes. Optimal duration of intensive care management has not been determined. Although we have an advanced understanding of the pathophysiology and clinical characteristics of subarachnoid hemorrhage, there are many controversies in the intensive care unit management of subarachnoid hemorrhage. With an awareness of not only delayed cerebral ischemia but also early brain injury, more attention should be given to various aspects to improve neurological outcomes.

In patients with aneurysmal subarachnoid hemorrhage (SAH), increased glucose variability (GV) is associated with increased mortality and cerebral infarction; however, there are no reports demonstrating an association between GV and neurological outcome. This study investigated whether GV had an independent effect on neurological outcomes in patients with SAH in the intensive care unit. Consecutive adult patients hospitalized with SAH between January 1, 2009, and May 31, 2015 (N = 122) were retrospectively reviewed. Univariate/multivariate analyses were performed to identify independent predictors of poor neurological outcome. Patients were divided according to the mean glucose level (80-139 vs 140-200 mg/dL) and further subdivided using quartiles (Q) of the standard deviation (SD, representing variability) of the glucose level (Q1, Q2 + 3, and Q4). Unfavorable neurological outcomes occurred in 44.2% of the patients. On multiple regression analysis, age, Hunt and Kosnik grade, SD of glucose (odds ratio [OR], 1.09; 95% confidence interval [CI], 1.02-1.17; P < .01), and minimum blood glucose level (OR, 0.95; 95% CI, 0.91-0.99; P < .01) were significantly associated with unfavorable neurological outcomes. Both groups (mean glucose levels: 80-139 and 140-200 mg/dL groups) had increasing unfavorable neurological outcomes with increasing SD of glucose (Q1, 15.0%; Q2 + 3, 40.0%; Q4, 52.4% and Q1, 44.4%; Q2 + 3, 50%; Q4, 88.9% in the 80-139 and 140-200 mg/dL groups, respectively). Patients with minimum glucose of 50% of unfavorable neurological outcome. Increased GV was an independent predictor of unfavorable neurological outcomes in patients with SAH.

Introduction: Dysnatremia commonly occur in the intensive care unit (ICU) management of patients with aneurysmal subarachnoid hemorrhage (SAH). However, detailed management strategies have not been provided even by current guidelines. The purposes of this study were to examine the association of abnormal serum sodium levels with unfavorable neurologic outcomes and to identify the target range of serum sodium in patients with SAH. Methods: We retrospectively reviewed all patients who were consecutively hospitalized with a confirmed diagnosis of SAH between January 2009 and December 2015. Univariate/multivariate analyses were performed to identify the independent predictors of an unfavorable neurologic outcome (modified Rankin scale of 3–6 upon hospital discharge). Results: There were 131 patients included in this study. Unfavorable neurologic outcomes occurred in 45% of patients. On multiple regression analysis, age, Hunt and Kosnik grade, and serum sodium levels in the ICU at the maximum [odds ratio (OR), 1.18; 95% CI, 1.05–1.35; P < 0.01] and minimum (OR, 0.88; 95% CI, 0.77–0.99; P = 0.048) values were significantly associated with unfavorable neurologic outcomes. The receiver operating characteristic curve analysis showed that the cut-off serum sodium levels were 145 mmol/L for maximum value and 132 mmol/L for minimum value. Patients with hyponatremia and hypernatremia during the first 2 weeks in the ICU accounted for 88.2% of patients with an unfavorable neurologic outcome; whereas, those with normal sodium levels accounted for only 15.6%. Conclusions: In patients with SAH, both hyponatremia and hypernatremia during ICU management were significantly associated with unfavorable neurologic outcomes.

The International Liaison Committee on Resuscitation guidelines recommend target temperature management (TTM) between 32 and 36 °C for patients after out-of-hospital cardiac arrest, but did not indicate patient-specific temperatures. The association of serum lactate concentration and neurological outcome in out-of-hospital cardiac arrest patient has been reported. The study aim was to investigate the benefit of 32–34 °C in patients with various degrees of hyperlactatemia compared to 35–36 °C. This study was a post hoc analysis of the Japanese Association for Acute Medicine out-of-hospital cardiac arrest registry between June 2014 and December 2015. Patients with complete targeted temperature management and lactate data were eligible. Patients were stratified to mild (< 7 mmol/l), moderate (< 12 mmol/l), or severe (≥ 12 mmol/l) hyperlactatemia group based on lactate concentration after return of spontaneous circulation. They were subdivided into 32–34 °C or 35–36 °C groups. The primary endpoint was an adjusted predicted probability of 30-day favorable neurological outcome, defined as a cerebral performance category score of 1 or 2. Of 435 patients, 139 had mild, 182 had moderate, and 114 had severe hyperlactatemia. One hundred and eight (78%) with mild, 128 with moderate (70%), and 83 with severe hyperlactatemia (73%) received TTM at 32–34 °C. The adjusted predicted probability of a 30-day favorable neurological outcome following severe hyperlactatemia was significantly greater with 32–34 °C (27.4%, 95% confidence interval: 22.0–32.8%) than 35–36 °C (12.4%, 95% CI 3.5–21.2%; p = 0.005). The differences in outcomes in those with mild and moderate hyperlactatemia were not significant. In OHCA patients with severe hyperlactatemia, the adjusted predicted probability of 30-day favorable neurological outcome was greater with TTM at 32–34 °C than with TTM at 35–36 °C. Further evaluation is needed to determine whether TTM at 32–34 °C can improve neurological outcomes in patients with severe hyperlactatemia after out-of-hospital cardiac arrest.