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Aim: We evaluated serum tau protein as biomarker for poor neurological outcome over an extended observation period in patients after successful cardiopulmonary resuscitation (CPR) treated with mild therapeutic hypothermia (MTH) or normothermia (NT)., Methods: This is a retrospective analysis of a prospective observational study including 132 patients after successful CPR. Serum tau was determined in 24 h intervals for up to 168 h after CPR. Patients were treated with MTH targeting a temperature of 33 °C for 24 h or NT according to current guidelines. Neurological outcome was assessed with the Cerebral Performance Categories Scale (CPC) at hospital discharge., Results: Forty-three percent of the patients were treated with MTH. Serial serum tau levels (pg/ml) showed a peak between 72-96 h after CPR (159 (IQR 27-625). Patients with poor neurological outcome (CPC 3-5) at hospital discharge (n = 68) had significantly higher serum tau levels compared to patients with good neurological outcome at 0-24 h (164 (48-946) vs. 69 (12-224); p = 0.009), at 24-48 h (414 (124-1049) vs. 74 (0-215); p < 0.001), at 48-72 h (456 (94-1225) vs. 69 (0-215); p < 0.001) and at 72-96 h (691 (197-1173) vs. 73 (0-170); p < 0.001). At 72-96 h the AUC to predict poor neurological outcome was 0.848 (95% CI: 0.737-0.959). Serum tau levels were not significantly different between patients with MTH and NT in multivariate analysis after adjusting for clinical relevant covariates., Conclusion: Serum tau showed highest values and the best prognostic discrimination of poor neurological outcome at 72-96 h after CPR. Prolonged elevation may indicate ongoing axonal damage in patients with hypoxic encephalopathy., (Copyright © 2020. Published by Elsevier B.V.)

Objective: To investigate the dynamic change in the serum Tau protein early after acute traumatic brain injury (TBI) and its association with neurological outcome and cognitive function., Subjects and Methods: Around 229 patients with acute TBI and 30 healthy subjects were evaluated for the serum levels of Tau protein on 1, 3, 5, 7, and 14 days after TBI. The relationships of the serum levels of Tau protein and initial GCS and GOS at 6 months post-injury were also analyzed. Further, 95 TBI patients were assessed with their cognitive function with Montreal cognitive assessment (MoCA) score., Results: Serum Tau was significantly higher in patients with TBI at 1, 3, 5, 7, and 14 days. The serum Tau at each point was significantly lower respectively in the patients with mild TBI than that in medium and severe TBI. The serum Tau was significantly lower in patients with good outcome compared to the poor outcome group. The early serum Tau was negatively correlated with both GCS and GOS. In the TBI group, 39 (41%) out of 95 patients developed cognitive dysfunction assessed by MoCA. Tau protein at day 1, 3, and 5 after TBI was significantly correlated with cognitive dysfunction at 6 months after TBI., Conclusions: Acute Tau associations with neurological outcomes and cognition may implicate white matter damage and neuronal degeneration. Serum Tau may be used as a reliable biological marker for early diagnosis and cognitive recovery following TBI.

Objective: Exposure to hyperoxemia and hypoxemia is common in out-of-hospital cardiac arrest (OHCA) patients following return of spontaneous circulation (ROSC), but its effects on neurological outcome are uncertain, and study results are inconsistent., Methods: Exploratory post hoc substudy of the Target Temperature Management (TTM) trial, including 939 patients after OHCA with return of spontaneous circulation (ROSC). The association between serial arterial partial pressures of oxygen (PaO 2 ) during 37 h following ROSC and neurological outcome at 6 months, evaluated by Cerebral Performance Category (CPC), dichotomized to good (CPC 1-2) and poor (CPC 3-5), was investigated. In our analyses, we tested the association of hyperoxemia and hypoxemia, time-weighted mean PaO 2 , maximum PaO 2 difference, and gradually increasing PaO 2 levels (13.3-53.3 kPa) with poor neurological outcome. A subsequent analysis investigated the association between PaO 2 and a biomarker of brain injury, peak serum Tau levels., Results: Eight hundred sixty-nine patients were eligible for analysis. Three hundred patients (35%) were exposed to hyperoxemia or hypoxemia at some time point after ROSC. Our analyses did not reveal a significant association between hyperoxemia, hypoxemia, time-weighted mean PaO 2 exposure or maximum PaO 2 difference and poor neurological outcome at 6-month follow-up after correction for co-variates (all analyses p = 0.146-0.847). We were not able to define a PaO 2 level significantly associated with the onset of poor neurological outcome. Peak serum Tau levels at either 48 or 72 h after ROSC were not associated with PaO 2 ., Conclusion: Hyperoxemia or hypoxemia exposure occurred in one third of the patients during the first 37 h of hospitalization and was not significantly associated with poor neurological outcome after 6 months or with the peak s-Tau levels at either 48 or 72 h after ROSC.

Background: Dyscarbia is common in out-of-hospital cardiac arrest (OHCA) patients and its association to neurological outcome is undetermined., Methods: This is an exploratory post-hoc substudy of the Target Temperature Management (TTM) trial, including resuscitated OHCA patients, investigating the association between serial measurements of arterial partial carbon dioxide pressure (PaCO 2 ) and neurological outcome at 6 months, defined by the Cerebral Performance Category (CPC) scale, dichotomized to good outcome (CPC 1 and 2) and poor outcome (CPC 3-5). The effects of hypercapnia and hypocapnia, and the time-weighted mean PaCO 2 and absolute PaCO 2 difference were analyzed. Additionally, the association between mild hypercapnia (6.0-7.30 kPa) and neurological outcome, its interaction with target temperature (33 °C and 36 °C), and the association between PaCO 2 and peak serum-Tau were evaluated., Results: Of the 939 patients in the TTM trial, 869 were eligible for analysis. Ninety-six percent of patients were exposed to hypocapnia or hypercapnia. None of the analyses indicated a statistical significant association between PaCO 2 and neurological outcome (P = 0.13-0.96). Mild hypercapnia was not associated with neurological outcome (P = 0.78) and there was no statistically significant interaction with target temperature (P interaction  = 0.95). There was no association between PaCO 2 and peak serum-Tau levels 48 or 72 h after return of spontaneous circulation (ROSC)., Conclusions: Dyscarbia is common after ROSC. No statistically significant association between PaCO 2 in the post-cardiac arrest phase and neurological outcome at 6 months after cardiac arrest was detected. There was no significant interaction between mild hypercapnia and temperature in relation to neurological outcome.