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Gray matter (GM) atrophy and white matter (WM) lesions may contribute to cognitive decline in patients with delayed neurological sequelae (DNS) after carbon monoxide (CO) poisoning. However, there is currently a lack of evidence supporting this relationship. This study aimed to investigate the volume of GM, cortical thickness, and burden of WM lesions in 33 DNS patients with dementia, 24 DNS patients with mild cognitive impairment, and 51 healthy controls. Various methods, including voxel‐based, deformation‐based, surface‐based, and atlas‐based analyses, were used to examine GM structures. Furthermore, we explored the connection between GM volume changes, WM lesions burden, and cognitive decline. Compared to the healthy controls, both patient groups exhibited widespread GM atrophy in the cerebral cortices (for volume and cortical thickness), subcortical nuclei (for volume), and cerebellum (for volume) ( p  < .05 corrected for false discovery rate [FDR]). The total volume of GM atrophy in 31 subregions, which included the default mode network (DMN), visual network (VN), and cerebellar network (CN) ( p  < .05, FDR‐corrected), independently contributed to the severity of cognitive impairment ( p  < .05). Additionally, WM lesions impacted cognitive decline through both direct and indirect effects, with the latter mediated by volume reduction in 16 subregions of cognitive networks ( p  < .05). These preliminary findings suggested that both GM atrophy and WM lesions were involved in cognitive decline in DNS patients following CO poisoning. Moreover, the reduction in the volume of DMN, VN, and posterior CN nodes mediated the WM lesions‐induced cognitive decline.

Delayed neurological sequelae (DNS) is a devastating consequence following acute carbon monoxide (CO) poisoning. This study aims at exploring the independent predictors of DNS in patients with CO exposure. Data of patients with diagnosis of CO poisoning was retrospectively collected and reviewed in 5 regional medical facilities. Patients were classified into the DNS group and non-DNS group according to clinical findings during a follow-up period of 6 months. Demographic characteristics, co-morbidities, clinical manifestations, and treatment strategies were compared to identify possible correlative factors. Multivariate analysis was performed to determine the independent predictors of DNS. We screened 1129 patients and enrolled 326 cases (158 males, average age 44.56 ± 16.08 years) in the analysis. Thirty-seven (11.35%) developed DNS at a median interval of 33 days. Uni-variable analysis identified older age, higher body mass index, hypertension, loss of consciousness, longer CO exposure, lower Glasgow Coma Scale (GCS) on-site/at emergency room, and elevation of lactate as relevant factors for DNS; while multivariable logistic regression revealed that older age (OR = 1.11; p < 0.001), longer duration of CO exposure (OR = 1.54; p = 0.023), GCS on-site (OR = 2.06; p < 0.001), and GCS at emergency room (OR = 1.33; p = 0.048) were independent predictors for DNS. Our multicenter study demonstrated older age, longer duration of CO exposure, and GCS score were independent predictors of DNS in COP patients. GCS scored on-site might be a more sensitive and specific parameter compared with GCS evaluated at the emergency room. Further prospective studies in a larger patient cohort are warranted to draw a comprehensive conclusion.

The main objective of the treatment of acute carbon monoxide (CO) poisoning is to prevent delayed neurological sequelae (DNS). However, today there is still no objective screening tool to identify patients at high risk of developing DNS. The aim of this study was to identify clinical factors that could predict DNS after acute charcoal-burning CO poisoning. This prospective observational study was conducted from September 1, 2019 to August 31, 2020 in a single academic medical center. Patients older than 18 years of age suffering from charcoal-burning CO poisoning were included in the study. After acute recovery, patients were followed up for six weeks to investigate for DNS development. The clinical predictors of DNS were determined using a multivariate logistic regression model. Of the 217 patients—113 males (52.1%), median age 37.0 (27.5–51.5) years—included, 49 (22.6%) developed DNS. The multivariate logistic regression analysis revealed the independent predictors of DNS as a lower initial Glasgow Coma Scale (GCS) score (adjusted odds ratio (AOR): 0.73, 95% confidence interval (CI): 0.62–0.87), a longer duration of CO exposure (AOR: 2.18, 95% CI: 1.65–2.88), and the presence of acute brain lesions with high signal intensity on diffusion-weighted imaging (AOR: 5.22, 95% CI: 1.50–18.08). The created multivariate regression model predicted DNS development with high accuracy (area under the curve: 0.93, 95% CI: 0.89–0.97). A low initial GCS score, longer exposure to CO and abnormal findings on diffusion-weighted magnetic resonance imaging can assist in the early identification of patients at high risk of DNS development.

Purpose: To investigate whether altered functional activity, functional connectivity (FC), and structural connectivity (SC) following acute carbon monoxide (CO) poisoning contribute to delayed neurological sequelae (DNS) occurrence. Methods: Binary degree centrality (DC) and seed-based FC were investigated in 18 patients with DNS, 26 patients without DNS, and 30 healthy controls. Duration of CO exposure and coma severity indices-related fibers was detected by connectometry analysis and the identified fiber tracts were tracked and their SC alteration was quantify by fractional anisotropy (FA). Results: Acute CO exposure induced DC change in the prefrontal cortex (PFC), visual cortex, primary sensory cortex, and anterior cerebellum, and FC alteration between the right fusiform gyrus (seed) and bilateral PFC and left inferior occipital gyrus (Gaussian random field corrected, P  < 0.05). Poisoning severity indices-related WM fibers consisted of corpus callosum and some association and projection fibers (false discovery rate corrected, P  < 0.05). Only altered DC in the right fusiform gyrus and right postcentral gyrus and reduced FC of the PFC could identify DNS occurrence ( P  < 0.05). Conclusions: The functional abnormalities in the visual- and sensory- cortex and PFC subsequent to acute CO poisoning represent one of the potential neural mechanisms underlying the occurrence of DNS.

Purpose To investigate early neurological deficits-related change patterns in gray matter (GM) volume in patients with carbon monoxide poisoning (COP) and GM volume differences between patients with and without delayed neurological sequelae (DNS) and those with and without T2 hyperintense lesions after COP. Methods Forty-one COP patients (24 patients with DNS) and 36 sex- and age-matched healthy controls (HC) were enrolled in this study. The neurological assessments were administered within 24 h after MRI scans. Voxel-based morphometry analysis was used to detect regional GM volume change. Results The COP group had statistically significant GM atrophy in the bilateral prefrontal and temporal lobes, anterior cingulate (ACC), thalamus, posterior cerebellum, and right hippocampus compared to the HC group. Atrophy in the left medial orbital superior frontal gyrus (SFG), bilateral ACC, and bilateral thalamus were related to lower Mini-Mental State Examination (MMSE) scores and higher Unified Parkinson’s Disease Rating Scale subsection III and neuro-psychiatric inventory scores. Atrophy in the hippocampus and posterior cerebellum were also related to decrease MMSE scores. The DNS subgroup had greater GM atrophy in the limbic system than the non-DNS subgroup. Compared to the subgroup without T2 hyperintense lesions, greater GM atrophy in the limbic system, motor and visual cortex, and default network was observed in the subgroup with T2 hyperintense lesions. Conclusion GM atrophy in the medial orbital SFG, ACC, thalamus, hippocampus, and posterior cerebellum is associated with early neurological deficits in patients with COP. Greater atrophy occurred in patients with DNS and those with T2 hyperintense lesions.

Delayed neurological sequelae (DNS) are a severe complication of carbon monoxide poisoning (COP) and high predisposing rates of disability and mortality, yet the relationship between exposure factors and DNS remains unknown. The aim was to investigate the association between domestic sources of COP and DNS. Patients diagnosed with COP between December 2016 and November 2021 were included and divided into two groups according to their sources of poisoning and the endpoint outcome was analyzed by logistic regression before and after propensity score matching (PSM). Overall, medical data from 314 patients were analyzed. In multivariate logistic regression, advanced age (adjusted odds ratio (AOR): 1.028, 95% CI: 1.008–1.049, P = 0.007), longer duration of exposure to the first treatment of hyperbaric oxygen (HBO) (AOR: 1.081, 95% CI: 1.036–1.127, P = 0.001), and intoxication by charcoal burning (AOR: 3.24, 95% CI: 1.208–8.69, P = 0.019) were associated with a higher risk of developing DNS. After 1:1 PSM, the outcomes also revealed that charcoal burning intoxication (odds ratio (OR): 8.396, 95% CI: 3.342–21.095, P<0.001) was associated with greater odds of DNS. This study indicates that domestic COP caused by charcoal burning is more likely to trigger DNS than gas-emitting heaters.

Carbon monoxide (CO) has been the leading cause of poisoning mortality in many countries and hyperbaric oxygen (HBO) is a widely accepted treatment for CO poisoning. However, some patients with CO poisoning will still develop neurocognitive sequelae regardless of HBO therapy, which can persist since CO poisoning or be present days to weeks after a recovery from CO poisoning. HBO has been used in the prevention and treatment of neurocognitive sequelae after CO poisoning, and some mechanisms are also proposed for the potential neuroprotective effects of HBO on the neurocognitive impairment after CO poisoning, but there is still controversy on the effectiveness of HBO on neurocognitive sequelae after CO poisoning. In this paper, we briefly introduce the neurocognitive sequelae after CO poisoning, summarize the potential predictive factors of neurocognitive sequelae, and discuss the use of HBO in the treatment and prevention of neurocognitive sequelae after CO poisoning.

To establish and validate a predictive formula for calculating the possibility of developing delayed neurological sequelae (DNS) after acute carbon monoxide (CO) poisoning to facilitate better decision-making about treatment strategies. This study retrospectively enrolled 605 consecutive patients who had been newly diagnosed with CO poisoning from the Central Hospital of Enshi Prefecture between January 1, 2015 and December 31, 2020. The cohort was randomly divided into two subgroups: the development cohort (n = 104) and validation cohort (n = 44). Univariate analysis and backward elimination of multivariate logistic regression were used to identify predictive factors, and a predictive formula was established. The performance was assessed using the area under the curve (AUC), the mean AUC of five-fold cross-validation, and calibration plots. The formula included four commonly available predictors: initial GCS score, duration of exposure, CK, and abnormal findings on MRI. We next created a formula to calculate the risk score for developing DNS: Risk score = −4.54 + 3.35 * (Abnormal findings on MRI = yes) - 0.51 * (Initial GCS score) + 0.65 * (Duration of exposure) + 0.01 * (CK). Then, the probability of developing DNS could be calculated: Probability of DNS = 1/(1 + e Risk score). The model revealed good discrimination with AUC, and mean AUC of fivefold cross-validation in two cohort, and the calibration plots showed good calibration. This study established a prediction predictive formula for predicting developing of DNS, which could facilitate better decision-making about treatment strategies. •Despite the predictive factors were identified, there are no models to predict delayed neurological sequelae.•A predictive formula was established, which can be used to calculate probability of delayed neurological sequelae.•The model showed good discrimination, calibration and generalizability When applied to internal validation.

AbstractBackground:Carbon monoxide (CO) poisoning remains a major cause of accidental injuries and multiple studies have indicated that CO is also associated with significantly severe or long-term toxicity to the central nervous system. Given that CO poisoning causes serious morbidity and mortality, a better understanding of epidemiological features and clinical characteristics of acute CO poisoning in China is crucial.Methods:We collected the clinical data of acute CO poisoning in patients between November 2019 and April 2020 across Shandong province, China and analyzed its characteristics focusing on the weekly amount and the severity of the confirmed cases.Results:A total number of 21,088 acute CO poisoning cases were diagnosed. The overall incidence of acute CO poisoning was approximately 0.021%. On severity rankings, 63% of confirmed cases (n = 13,378) were mild, 27% (n = 5635) were moderate, and 10% (n = 2075) were severe. Interestingly, the coastal cities had more confirmed cases than the inland/suburban areas in Shandong. Meanwhile, the number of confirmed cases was negatively correlated with the local mean daily temperature (P = 0.0167).Conclusions:Mild acute CO poisoning cases accounted for the majority of all confirmed cases during the winter of 2019. In Shandong province, which is located in east China, residents of the coastal cities are more susceptible to CO poisoning than residents of inland cities.

Carbon monoxide (CO) is a colorless, odorless gas and tasteless. CO poisoning (COP) is one of the most frequently encountered inhalation poisonings. The most common cause of morbidity in COP is delayed neurological sequelae (DNS). DNS is the occurrence of neuropsychiatric findings within 2–240 days after discharge of patients with COP and there are no definitive diagnostic criteria. The aim of our study is; to determine the risk factors and incidence of DNS. Our study is a retrospective, observational study. Patients with the diagnosis of COP in the emergency department between 2015 and 2016 were included in the study. Patients age, gender, findings in the initial physical examination (PE) and neurological examination (NE), blood carboxyhemoglobin (COHb) level, relation between hyperbaric oxygen (HBO) treatment and DNS were assessed. Total of 72 patients were included in the study. Mean age was 33.43 ± 20.89. It was determined that pathological findings in the initial NE are a significant predictive factor for DNS (Odds ratio 18.600, p:0.004). Significant relation between NE and HBO treatment was present (p:00.1). There was no statistically significant relationship between initial COHb level and receiving HBO treatment (p:0.9). Median COHb level of patients with DNS was 30 (min:10, max: 43), median COHb level of patients without DNS was 25 (min:10, max:44) and there was no statistically significant relationship between the two groups according to COHb levels (p:0.7). Pathological findings in the initial neurological examination had a predictive value for delayed neurological sequelae in patients with carbon monoxide poisoning.