Cerebral Glucose Metabolism following TBI: Changes in Plasma Glucose, Glucose Transport and Alternative Pathways of Glycolysis-A Translational Narrative Review.

Traumatic brain injury (TBI) is a major public health concern with significant consequences across various domains. Following the primary event, secondary injuries compound the outcome after TBI, with disrupted glucose metabolism emerging as a relevant factor. This narrative review summarises the existing literature on post-TBI alterations in glucose metabolism. After TBI, the brain undergoes dynamic changes in brain glucose transport, including alterations in glucose transporters and kinetics, and disruptions in the blood-brain barrier (BBB). In addition, cerebral glucose metabolism transitions from a phase of hyperglycolysis to hypometabolism, with upregulation of alternative pathways of glycolysis. Future research should further explore optimal, and possibly personalised, glycaemic control targets in TBI patients, with GLP-1 analogues as promising therapeutic candidates. Furthermore, a more fundamental understanding of alterations in the activation of various pathways, such as the polyol and lactate pathway, could hold the key to improving outcomes following TBI.

The role of intraoperative hypotension on the development of postoperative cognitive dysfunction: a systematic review.

STUDY OBJECTIVE: To clarify whether intraoperative hypotension contributes to the development of postoperative cognitive dysfunction. DESIGN: A systematic review of prospective studies reporting on intraoperative hypotension and postoperative cognitive dysfunction in elective, non-cognitive impaired, adult surgical patients. PubMed, EMBASE and the Cochrane Library were searched up to the 1st of January 2021. SETTING: Studies had to use a clear definition of hypotension, although differing definitions were accepted. Neurocognitive tests to determine postoperative cognitive dysfunction had to be done pre- and postoperatively, with a minimum follow-up of seven days postoperatively. MEASUREMENTS: Risk of bias was assessed using the Cochrane Risk of Bias Tool 2.0 for randomized controlled trials and the Newcastle-Ottawa Scale for cohort studies. MAIN RESULTS: Out of 941 studies screened, five randomized controlled trials and four cohort studies were included for qualitative analysis. Extensive methodological differences between studies were present hindering proper quantitive analysis. No studies reported statistically significant differences in incidence of postoperative cognitive dysfunction in hypo- compared to normotensive patients. Five studies reported exact incidences of postoperative cognitive dysfunction. CONCLUSIONS: This systematic review showed no conclusive association between intraoperative hypotension and the development of postoperative cognitive dysfunction. Given the vast methodological differences of the included studies, the role of intraoperative hypotension in the development of postoperative cognitive dysfunction remains uncertain. Future research into the association between intraoperative hypotension and postoperative cognitive dysfunction should be conducted in a standardized manner.