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In this prospective observational pilot study patients with the diagnosis of end-stage lung disease and listed for lung transplantation underwent a cognitive function test battery before and after lung transplantation to investigate postoperative cognitive function in three domains (visual and verbal memory, executive functioning, concentration/speed of processing). Additionally we investigated intraoperative risk factors for postoperative cognitive dysfunction. In total, 24 patients were included in this pilot study. The incidence of postoperative cognitive dysfunction was 58.3%. In the cognitive dysfunction group, the domains executive functioning and concentration/attention were significantly impaired whereas memory was not affected. Patients with cognitive impairment had a significantly longer ICU stay. The strongest independent risk factor for the development of cognitive dysfunction was operation time. No influence of cerebral oxygen desaturations on cognitive dysfunction was found. This might have important implications for early psychological rehabilitation strategies in this high-risk patient collective.

Postoperative cognitive dysfunction (POCD) has been increasingly recognized as a contributor to postoperative complications. A consensus-working group recommended that POCD should be distinguished between delayed cognitive recovery, ie, evaluations up to 30 days postoperative, and neurocognitive disorder, ie, assessments performed between 30 days and 12 months after surgery. Additionally, the choice of the anesthetic, either inhalational or total intravenous anesthesia (TIVA) and its effect on the incidence of POCD, has become a focus of research. Our primary objective was to search the literature and conduct a metaanalysis to verify whether the choice of general anesthesia may impact the incidence of POCD in the first 30 days postoperatively. As a secondary objective, a systematic review of the literature was conducted to estimate the effects of the anesthetic on POCD between 30 days and 12 months postoperative. For the primary objective, an initial review of 1913 articles yielded ten studies with a total of 3390 individuals. For the secondary objective, four studies with a total of 480 patients were selected. In the first 30 days postoperative, the odds-ratio for POCD in TIVA group was 0.46 (95% CI = 0.26-0.81; p = 0.01), compared to the inhalational group. TIVA was associated with a lower incidence of POCD in the first 30 days postoperatively. Regarding the secondary objective, due to the small number of selected articles and its high heterogeneity, a metanalysis was not conducted. Given the heterogeneity of criteria for POCD, future prospective studies with more robust designs should be performed to fully address this question. Keywords: postoperative cognitive dysfunction, POCD, total intravenous anesthesia, TIVA, inhalational anesthesia, postoperative complications, psychometric tests

Background: Postoperative cognitive dysfunction (POCD) is a common postoperative complication in elderly patients. The purpose of this study was to investigate the mechanism through which metformin improves postoperative cognitive function. Methods: In the in vivo experiment, 18-month-old Sprague–Dawley (SD) rats were randomly divided into four groups (n = 12 in each group): the control, metformin, operation, and operation plus metformin groups. The animals were pretreated with metformin by gavage once daily for two weeks. The Morris water maze (MWM) was used to measure cognitive ability. In the in vitro experiment, BV2 cells were divided into five groups: the control, metformin, lipopolysaccharide (LPS), LPS plus metformin, and LPS plus metformin plus compound C groups. We stimulated microglia with LPS (500 ng/mL). Immunofluorescence and Western blotting were used to assess ROS (reactive oxygen species) levels, autophagy-associated protein levels and adenosine monophosphate-activated protein kinase (AMPK)/regulator factor 2-related enzyme 1 (SIRT1) signaling pathway activity in the rat cortex and microglial cells. Results: In the MWM test, the metformin-pretreated rats spent a higher proportion of time in the target quadrant. Immunofluorescence showed that the fluorescence intensity of LC3 in the cortex was increased in rats pretreated with metformin. Western blotting indicated that metformin upregulated the expression of autophagy-related and AMPK/SIRT1 signaling pathway-related proteins in the cortex after surgery. By activating the AMPK/SIRT1 signaling pathway in vitro, metformin reduced microglial activation and oxidative stress and promoted autophagy. Conclusions: Through the AMPK/SIRT1 pathway, metformin can boost autophagy and reduce oxidative stress in cortical microglia in older rats, in turn improving postoperative cognitive function.

Postoperative cognitive dysfunction (POCD) appears in up to 30% of patients suffering from postoperative delirium (POD). Both are associated with higher mortality and postoperative complications, prolonged hospital stays, and increased costs. Multi-modal models with pre-admission risk reduction counselling, perioperative monitoring, and training of multidisciplinary patient care providers have been shown to decrease the prevalence of both. The aim of our study is to understand how far those measures are known and implemented in routine care and to detect potential gaps in the current practice regarding risk communication and information flow between involved caregivers for patients at risk for POD/POCD. As part of a multicenter study, seven semi-structured focus group (FG) discussions with nurses and physicians from tertiary care hospitals (surgery, anesthesiology, and orthopedics, n=31) and general practitioners (GPs) in private practice (n=7) were performed. Transcribed discussions were analyzed using qualitative content analysis. POD is present above all in the daily work of nurses, whereas physicians do not perceive it as a relevant problem. Physicians report that no regular risk assessment or risk communication was performed prior to elective surgery. Information about POD often gets lost during hand-offs and is not regularly reported in discharge letters. Thus, persisting cognitive dysfunction is often missed. The importance of standardized documentation and continuous education concerning risks, screening, and treatment was emphasized. The often-suggested pre-OP medication adjustment was seen as less important; in contrast, avoiding withdrawal was regarded as far more important. Altogether, it seems that standards and available best practice concepts are rarely implemented. In contrast to physicians, nurses are highly aware of delirium and ask for standardized procedures and more responsibility. Therefore, raising awareness regarding risks, screening tools, and effective preventive measures for POD/POCD seems an urgent goal. Nurses should have a central role in coordination and care of POD to prevent the risk for POCD.

Background: Patient satisfaction with anesthesia after surgical treatment is a complex concept that includes not only the level of satisfaction with the anesthesia itself but also the presence of fears, worries, depression, evaluation of the anesthesiologists' work, as well as cognitive dysfunction as a possible negative consequence of anesthesia. Objective: Conducting a comprehensive analysis of patients' satisfaction with anesthesia. Methods: Questionnaire of patients' satisfaction with anesthesia (Sinbukhova E.V., Lubnin A.Yu.), State-Trait Anxiety Inventory in the adaptation by Y.L. Hanin, Assessment of Depression, The Montreal Cognitive Assessment (MoCA), and Frontal Assessment Battery. Population consisted of 202 patients. Results: Satisfaction with anesthesia: assessment \"good and higher\" with primary anesthesia - 59.7% of patients with repeated - 70% of patients. The most common factors that reduce the assessment of patients' satisfaction with anesthesia are: strong excitement before surgery about operation and anesthesia, no postoperative visit of the anesthesiologist, no visit of the anesthesiologist before the operation, not enough attention of anesthesiologist in the surgery room before anesthesia, nausea, vomiting, pain, dizziness, general discomfort, and thirst. MoCA cognitive assessment before and after anesthesia: P < 2.2 e-16 (significant decrease). Depression: major depression in 52% of patients, subclinical depression in 22.8%. Conclusion: Regular survey of patients' satisfaction should help to improve the quality of medical care. The strong excitement of the patient about the upcoming anesthesia and surgery, and the presence of a high level of anxiety and depression can be factors of reducing the patients' satisfaction with anesthesia. It requires psychological support of patients at the stage of surgical treatment.

Despite vitamin D deficiency (VDD) associated with cognitive dysfunction in the general population, the impacts of preoperative VDD on postoperative delirium (POD) and cognitive dysfunction (POCD) remain to be clarified. Meta-analysis of cohort studies. Postoperative care. Preoperative VDD as the prognostic factor. Adult patients undergoing surgery. Databases including MEDLINE, EMBASE, Google scholar, and the Cochrane Library databases were searched from inception to September 2021. Random-effects modeling was applied to the pooling of results on the association between preoperative VDD and POD/POCD. The primary outcome was the association of VDD with the risk of POD/POCD, while the secondary outcomes included other prognostic factors (e.g., hypertension) with the risk of POD/POCD. A prediction interval (PI) was calculated to indicate the range of a true effect size of a future study in 95% of all populations. Meta-analysis of seven observational studies involving 2673 patients showed that the pooled incidence of POD/POCD was 29% (95% confidence interval (CI): 18% to 44%). Our results demonstrated that preoperative VDD increased the risk of POD/POCD [odds ratio (OR) = 1.54, 95% CI: 1.21–1.97, p < 0.01; I2 = 29.2%, seven studies, 2673 patients; 95% PI: 0.89–2.67], while vitamin D insufficiency was not associated with a higher risk of POD/POCD (OR = 0.88, 95% CI: 0.49–1.57, p = 0.66; I2 = 62.6%, four studies, 1410 patients; 95% PI: 0.09–8.79). The PI in our primary outcome (i.e., 0.89 to 2.67) containing 1.0 suggested the possibility of inconsistent results in future studies. Patients with POD/POCD were older compared to those without. Hypertension, diabetes mellitus, male gender, or smoking was not recognized as risk factors for POD/POCD. Our results demonstrated that preoperative vitamin D deficiency was associated with postoperative cognitive impairment. Given the prediction interval, more future studies are needed to elucidate associations between VDD and POD/POCD. •Postoperative delirium and cognitive dysfunction are postsurgical cognitive disorders.•Preoperative vitamin D deficiency increased postoperative cognitive disorders' risk.•Preoperative vitamin D deficiency remained a risk factor in subgroup analysis.•The meta-analysis results suggest optimization of preoperative vitamin D status.

Background Postoperative cognitive dysfunction (POCD) is a common neurological complication following anesthesia and surgery. Increasing evidence has demonstrated that neuroinflammation caused by systemic inflammatory responses during the perioperative period is a key factor in the occurrence of POCD. In addition, SMAD family member 7 (Smad7) has been confirmed to play vital roles in the pathogenesis and treatment of inflammatory diseases, such as inflammatory bowel disease. However, whether Smad7 participates in the regulatory process of neuroinflammation and apoptosis in the development of POCD is still unknown. Methods In this study, a POCD mouse model was constructed by unilateral nephrectomy under anesthesia, and cognitive function was assessed using the fear conditioning test and open field test. The expression of Smad7 at the mRNA and protein levels in the hippocampus 3 days after surgery was examined by qRT-PCR, western blot and immunofluorescence assays. Furthermore, to identify whether the elevation of Smad7 in the hippocampus after unilateral nephrectomy contributes to cognitive impairment, the expression of Smad7 in the hippocampal CA1 region was downregulated by crossing Smad7 fl/fl conditional mutant mice and CaMKIIα-Cre line T29-1 transgenic mice or stereotaxic injection of shRNA–Smad7. Inflammation and apoptosis in the hippocampus were assessed by measuring the mRNA levels of typical inflammatory cytokines, including TNF-α, IL-1β, IL-6, CCL2, CXCL1, and CXCL2, and the protein levels of apoptotic proteins, including Bax and Bcl2. In addition, apoptosis in the hippocampus postoperation was investigated by a terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) staining assay. Finally, western blotting was used to explore how Smad7 mediates inflammation and apoptosis postoperation. Results The results unequivocally revealed that elevated Smad7 in the hippocampal CA1 region significantly inhibited TGF-β signal transduction by blocking Smad2/3 phosphorylation, which enhanced neuroinflammation and apoptosis in the hippocampus and further led to learning and memory impairment after surgery. Conclusions Our results revealed that Smad7 contributes to cognitive impairment after surgery by enhancing neuroinflammation and apoptosis in the hippocampus and might serve as a promising therapeutic target for the treatment of memory impairment after anesthesia surgery.

Postoperative cognitive dysfunction (POCD) is common, occurring in around 10-54% of individuals within first few weeks after surgery. Although the majority of POCD is less commonly persistent later than 3 months following surgery, the condition increases length of stay (LOS), mortality and long-term cognitive decline, raising the need for a broad screening to identify individuals at risk for POCD during the perioperative period. In this narrative review, we summarize preoperative, intraoperative and postoperative risk factors for POCD reported in last 5 years and discuss neuropsychological tools and potential biomarkers and time points for assessment that might be suitable for clinical use. We aim to provide crucial information for developing a strategy of routine screening for POCD, which may assist with better identification of at-risk individuals for early interventions. Very importantly, the utilization of a standardized strategy may also allow higher consistency and comparability across different studies.

Postoperative cognitive dysfunction (POCD) is a frequent neurological complication encountered during the perioperative period with unclear mechanisms and no effective treatments. Recent research into the pathogenesis of POCD has primarily focused on neuroinflammation, oxidative stress, changes in neural synaptic plasticity and neurotransmitter imbalances. Given the high-energy metabolism of neurons and their critical dependency on mitochondria, mitochondrial dysfunction directly affects neuronal function. Additionally, as the primary organelles generating reactive oxygen species, mitochondria are closely linked to the pathological processes of neuroinflammation. Surgery and anesthesia can induce mitochondrial dysfunction, increase mitochondrial oxidative stress, and disrupt mitochondrial quality-control mechanisms via various pathways, hence serving as key initiators of the POCD pathological process. We conducted a review on the role and potential mechanisms of mitochondria in postoperative cognitive dysfunction by consulting relevant literature from the PubMed and EMBASE databases spanning the past 25 years. Our findings indicate that surgery and anesthesia can inhibit mitochondrial respiration, thereby reducing ATP production, decreasing mitochondrial membrane potential, promoting mitochondrial fission, inducing mitochondrial calcium buffering abnormalities and iron accumulation, inhibiting mitophagy, and increasing mitochondrial oxidative stress. Mitochondrial dysfunction and damage can ultimately lead to impaired neuronal function, abnormal synaptic transmission, impaired synthesis and release of neurotransmitters, and even neuronal death, resulting in cognitive dysfunction. Targeted mitochondrial therapies have shown positive outcomes, holding promise as a novel treatment for POCD.

Background Neuroinflammation plays a key role in the occurrence and development of postoperative cognitive dysfunction (POCD). Microglia, the resident immune cells in the brain, has been increasingly recognized to contribute to neuroinflammation. Although brain mast cells (MCs) are the “first responder” in the brain injury rather than microglia, little is known about the functional aspects of MCs-microglia interactions. Methods Male Sprague-Dawley (SD) rats were injected intracerebroventricular with MC stabilizer Cromolyn (100 μg/μl), MC stimulator C48/80 (1 μg/μl), or sterile saline 30 min before open tibial fracture surgery, and the levels of neuroinflammation and memory dysfunction were tested 1 and 3 days after surgery. In addition, the effect of activated MCs on microglia and neurons was determined in vitro. Results Tibial fracture surgery induced MCs degranulation, microglia activation, and inflammatory factors production, which initiated the acute brain inflammatory response and neuronal death and exhibited cognitive deficit. Site-directed preinjection of the “MCs stabilizer” disodium cromoglycate (Cromolyn) inhibited this effect, including decrease of inflammatory cytokines, reduced MCs degranulation, microglia activation, neuronal death, and improved cognitive function 24 h after the surgery. In vitro study, we found that the conditioned medium from lipopolysaccharide (LPS)-stimulated mast cells line (P815) could induce primary microglia activation through mitogen-activated protein kinase (MAPK) pathway signaling and subsequent production of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). In addition, the activated P815 could directly induce neuronal apoptosis and synapse injury with microglia independently. Cromolyn could inhibit P815 activation following improved microglia activation and neuronal loss. Conclusions These results implicate that activated MCs could trigger microglia activation and neuronal damage, resulting in central nervous system (CNS) inflammation, and communications of MCs with microglia and neuron could constitute a new and unique therapeutic target for CNS immune inflammation-related diseases.