Daily Anesthesiology Research Analysis

The perioperative management of patients using sodium-glucose cotransporter 2 inhibitors (SGLT2is) remains controversial. The US Food and Drug Administration currently recommends stopping SGLT2is for 3-4 days before surgery, irrespective of a diagnosis of diabetes mellitus. Other multisociety recommendations vary significantly in terms of SGLT2i management, perioperative monitoring, and mitigating strategies for euglycaemic diabetic ketoacidosis. This multidisciplinary consensus statement led by the Society for Perioperative Assessment and Quality Improvement (SPAQI) provides updated recommendations based on a modified Delphi process and supported by a systematic review of the literature. The recommendations include a tailored approach to management of SGLT2is perioperatively based on the presence of diabetes mellitus and other comorbidities, surgical and periprocedural dietary considerations, as well as monitoring and prevention strategies for euglycaemic diabetic ketoacidosis.

BACKGROUND: Carbon dioxide is a key determinant of cerebral blood flow and is needed to prevent secondary damage in neurocritical care; however, optimal targets across the heterogeneous spectrum of acute brain injury (ABI) remain to be elucidated. The aim of this study was to evaluate the association between arterial hypocapnia and mortality and neurological outcomes in adult patients with ABI. METHODS: Six electronic databases were systematically searched from inception to January 2025. Observational and randomized controlled trials comparing exposure to hypocapnia, defined as an arterial partial pressure of carbon dioxide (PaCO RESULTS: A total of 8,637 records were identified after duplicate removal, of which 37 studies met inclusion criteria for the systematic review. Twenty-seven studies (51,373 patients) were included for mortality outcomes, and thirteen studies (3,814 patients) were included for neurological outcomes. Hypocapnia was associated with higher odds of mortality in adult patients with ABI (OR 1.29, 95% CI 1.05-1.59). Subgroup analyses demonstrated variability across ABI types, with stronger associations observed in subarachnoid hemorrhage and ischemic stroke populations. Hypocapnia was also associated with increased odds of poor neurological outcomes (OR 2.09, 95% CI 1.24-3.54), particularly in the traumatic brain injury population. Subgroup analyses suggested that the association with neurological outcomes was more consistent in studies defining exposure as severe hypocapnia (PaCO CONCLUSIONS: Arterial hypocapnia was associated with increased mortality and poor neurological outcomes in adults with acute brain injury, although the evidence is predominantly observational and limited randomized data are available. These findings underscore the need for cautious, individualized PaCO

BACKGROUND: Postoperative delirium (POD) is a serious complication in elderly patients. Dexmedetomidine (DEX) can reduce POD incidence, but its neuroprotective mechanisms are unclear. This study investigated whether DEX alleviates POD-like phenotypes and whether hippocampal transcription factor EB (TFEB) contributes to this effect, with a focus on microglial lysosomal function. METHODS: An aged mouse POD model was established via laparotomy with visceral manipulation. Mice were assigned to Sham, POD, and POD+DEX groups. Behavioral tests assessed cognitive and affective functions. Hippocampal tissues were analyzed for neuroinflammation and lysosomal markers. Primary microglia were isolated for in vitro studies involving TFEB knockdown. RESULTS: DEX treatment significantly ameliorated POD-like behaviors and reduced hippocampal microglial activation and pro-inflammatory cytokine levels. DEX treatment was associated with increased lysosomal protein expression and promoted TFEB nuclear translocation in microglia, correlating with enhanced lysosomal gene transcription. In vitro, DEX increased lysosomal acidity and improved functional readouts in LPS-stimulated microglia in a TFEB-dependent manner, suggesting partial recovery of lysosome-dependent clearance. DEX also inhibited the NLRP3 inflammasome pathway, an effect substantially attenuated by TFEB knockdown. Mechanistically, DEX-mediated TFEB activation was associated with reduced mTOR activity. CONCLUSION: DEX mitigates POD-like phenotypes in aged mice, with evidence that TFEB activation in the hippocampus contributes to restoration of lysosomal function and attenuation of neuroinflammation. Microglia appear to be a key cellular compartment in this process. These findings suggest that enhancing lysosomal function may represent a potential target for POD.