Brain monitoring after cardiac arrest.

PURPOSE OF REVIEW: To describe the available neuromonitoring tools in patients who are comatose after resuscitation from cardiac arrest because of hypoxic-ischemic brain injury (HIBI). RECENT FINDINGS: Electroencephalogram (EEG) is useful for detecting seizures and guiding antiepileptic treatment. Moreover, specific EEG patterns accurately identify patients with irreversible HIBI. Cerebral blood flow (CBF) decreases in HIBI, and a greater decrease with no CBF recovery indicates poor outcome. The CBF autoregulation curve is narrowed and right-shifted in some HIBI patients, most of whom have poor outcome. Parameters derived from near-infrared spectroscopy (NIRS), intracranial pressure (ICP) and transcranial Doppler (TCD), together with brain tissue oxygenation, are under investigation as tools to optimize CBF in patients with HIBI and altered autoregulation. Blood levels of brain biomarkers and their trend over time are used to assess the severity of HIBI in both the research and clinical setting, and to predict the outcome of postcardiac arrest coma. Neuron-specific enolase (NSE) is recommended as a prognostic tool for HIBI in the current postresuscitation guidelines, but other potentially more accurate biomarkers, such as neurofilament light chain (NfL) are under investigation. SUMMARY: Neuromonitoring provides essential information to detect complications, individualize treatment and predict prognosis in patients with HIBI.

Monitoring and modifying brain oxygenation in patients at risk of hypoxic ischaemic brain injury after cardiac arrest.

This article is one of ten reviews selected from the Annual Update in Intensive Care and Emergency Medicine 2021. Other selected articles can be found online at https://www.biomedcentral.com/collections/annualupdate2021 . Further information about the Annual Update in Intensive Care and Emergency Medicine is available from https://link.springer.com/bookseries/8901 .

Early Moderate Hyperoxemia Does Not Predict Outcome After Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND: Targeting hyperoxemia is common practice in neurocritical care settings, but the safety of hyperoxemia has been questioned. OBJECTIVE: To investigate the independent effect of hyperoxemia on outcome in patients with aneurysmal subarachnoid hemorrhage (SAH). METHODS: We included 432 patients with aneurysmal SAH on mechanical ventilation for at least 24 hours after intensive care unit (ICU) admission. Arterial blood gas levels were calculated as time-weighted averages (TWAs) of all blood gas measurements during the first 24 hours in the ICU. Patients were categorized into 3 TWA-PaO2 bands (low, <97.5 mm Hg; intermediate, 97.5-150 mm Hg; high, ≥150 mm Hg). Outcome measures were unfavorable outcome at 3 months (Glasgow Outcome Scale score 1-3) and mortality. Multivariate logistic regression analysis was used to assess the independent effect of oxygen on outcome. RESULTS: Overall, 28% of patients died, and a total of 53% had an unfavorable outcome at 3 months. Patients with an unfavorable outcome had significantly higher TWA-PaO2 levels compared with patients with a favorable outcome (137 mm Hg vs 118 mm Hg, P < .001). Multivariate analysis demonstrated no significant association between TWA-PaO2 bands and unfavorable outcome (with intermediate PaO2 as a reference, odds ratio [OR] for low PaO2 1.05, 95% confidence interval [CI]: 0.52-2.12, P = .89; OR for high PaO2: 1.09, 95% CI: 0.61-1.97, P = .77) or mortality (with intermediate PaO2 as reference, the OR for low PaO2 was 0.67 (95% CI: 0.30-1.46, P = .31), and the OR for high PaO2 was 0.73 (95% CI: 0.38-1.40, P = .34). CONCLUSION: Early moderate hyperoxemia may not increase or decrease the risk of a poor outcome in mechanically ventilated aneurysmal SAH patients.

Copeptin levels are associated with organ dysfunction and death in the intensive care unit after out-of-hospital cardiac arrest.

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