Objective Patients undergoing spinal surgery in the prone position may experience venous stasis, often resulting in edema in dependent areas of the body, including the head, and increased postoperative cognitive dysfunction (POCD). Not only does POCD present challenges for post‐operative care and recovery, it can also cause permanent damage to the patient's brain and increase mortality and social costs. We aimed to clarify the incidence of POCD in patients with hypertension after prone spine surgery and to further determine the association between intraoperative somatic tissue oxygen saturation (SstO2)/cerebral tissue oxygen saturation (SctO2) and POCD. Methods Patients with hypertension scheduled for open prone spine surgery from January 2020 to April 2021 were included in this single‐center, prospective, observational study. SctO2 and SstO2 were monitored by near‐infrared spectroscopy continuously throughout the surgery. The primary outcome was POCD assessed using the Mini‐Mental Status Examination (MMSE). The association of SstO2 and SctO2 with POCD was evaluated with unadjusted analyses and multivariable logistic regression. Results One hundred and one of 112 identified patients were included, 28 (27.8%) of whom developed POCD. None of the investigated SctO2 indices were predictive of POCD. However, the patients with POCD had greater decreases in intraoperative absolute SstO2 and relative SstO2 than the patients without POCD (P = 0.037, P = 0.036). Moreover, three SstO2 indices were associated with POCD, including a greater absolute SstO2 decrease (P = 0.021), a greater relative SstO2 decrease (P = 0.032), and a drop below 90% of the baseline SstO2 (P = 0.002), independent of ASA III status, preoperative platelets and postoperative sepsis. In addition, there was no correlation between intraoperative SctO2 and intraoperative SstO2 or between their respective absolute declines. Conclusion Twenty‐eight (27.7%) of 101 patients developed POCD in patients with hypertension undergoing prone spine surgery, and intraoperative SstO2 is associated with POCD, whereas SctO2 shows no association with POCD. This study may initially provide a valuable new approach to the prevention of POCD in this population.

Background: Cognitive dysfunction after sepsis is the most serious complication after discharge of sepsis patients, and its pathogenesis is related to the inflammation of the central nervous system caused by the damaged blood-brain barrier. Interleukin-1β (IL-1β) is a key factor in sepsis-induced cognitive dysfunction in mice. Several investigations have suggested that TRPM2 (transient receptor potential melastatin-2) performs a vital task in immune response and inflammation. The aim of this exploration was to discover the importance of IL-1β in apoptosis in the hippocampal astrocytes of septic mice through in vitro and in vivo assessments. Methods: mouse severe inflammatory was established by intraperitoneal injection of high dose lipopolysaccharide (LPS, 5 mg kg–1), The Morris water maze task and fear conditioning test were used to investigate cognitive functions on the 7th day after LPS injection. Western blotting was implemented to detect the levels of IL-1β , TRPM2 and GFAP. Flow cytometry was employed to ascertain the effects of IL-1β and TRPM2-siRNA on the apoptosis of astrocytes. Immunofluorescent staining was used to examine the expression levels of GFAP and TRPM2 in hippocampus of mice .Results: Intraperitoneal injection of LPS caused cognitive dysfunction in mice, which can be reversed by down-regulation of IL-1β expression in the hippocampus. Elevated expression of IL-1β and TRPM2 were observed in hippocampus from the mouse after LPS injection. Specifc knockdown of IL-1β mRNA expression rescued the elevated expression of TRPM2. Accordingly, specifc knockdown of TRPM2 expression improved the cognitive impairment induced by Intraperitoneal injection of LPS.Conclusions: Elevated expression of IL-1β in the hippocampus may induce cognitive dysfunction by upregulation of TRPM2 in septic mice astrocytes.

Background: Intraoperative cerebral desaturations have been associated with worse neurological outcomes after supine surgery. However, it is not clear whether intraoperative somatic tissue oxygenation is more associated with postoperative cognitive dysfunction (POCD) than cerebral oxygenation in patients with hypertension after prone spine surgery.Methods: Patients with hypertension scheduled for spine open surgery were included from 2020 to 2021 in a single-center, prospective, observational study. Baseline both cerebral and somatic tissue oxygen saturation were measured in operating room before surgery. Cerebral and somatic tissue oxygen saturations were monitored continuously throughout surgery. The presence of POCD was assessed using the Mini-Mental Status Examination (MMSE). Association with POCD was evaluated with unadjusted analyses and multivariable logistic regression.Results: One hundred and one of 112 patients were included, and 28 (27.8%) developed POCD. None of the investigated SctO2 variables was predictive of POCD. On the contrary, the patients with POCD had a higher decrease in intraoperative absolute SstO2 decrease and relative SstO2 decrease compared with the patients without POCD (4.9%±3.8% vs. 3.6%±2.6%, P=0.037; 7.4%±5.6% vs. 5.3%±3.8%, P=0.036; respectively). Finally, three SstO2 parameters respectively were associated with POCD, including a higher absolute SstO2 decrease (OR, 1.223; 95%CI, 1.031-1.451; P=0.021), a higher absolute SstO2 decrease (OR, 1.138; 95%CI, 1.011-1.281; P=0.032) and falling below 90% of baseline SstO2 (OR, 11.388; 95%CI, 2.367-54.785; P=0.002), independent of ASA III, preoperative platelet and postoperative sepsis. Conclusions: Twenty-eight (27.8%) of 101patients developed POCD. Somatic tissue oxygenation has a stronger association with POCD than cerebral tissue oxygenation after spine open surgery in patients with hypertension.Clinical trial registration: ChiCTR1900028392. Registered 20 December 2019.