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Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. The clinical presentation runs a spectrum, ranging from headache and dizziness to coma and death, with a mortality rate ranging from 1 to 3%. A significant number of patients who survive CO poisoning suffer from long-term neurological and affective sequelae. The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. Long-term neurocognitive deficits occur in 15-40% of patients, whereas approximately one-third of moderate to severely poisoned patients exhibit cardiac dysfunction, including arrhythmia, left ventricular systolic dysfunction, and myocardial infarction. Imaging studies reveal cerebral white matter hyperintensities, with delayed posthypoxic leukoencephalopathy or diffuse brain atrophy. Management of these patients requires the identification of accompanying drug ingestions, especially in the setting of intentional poisoning, fire-related toxic gas exposures, and inhalational injuries. Conventional therapy is limited to normobaric and hyperbaric oxygen, with no available antidotal therapy. Although hyperbaric oxygen significantly reduces the permanent neurological and affective effects of CO poisoning, a portion of survivors still have substantial morbidity. There has been some early success in therapies targeting the downstream inflammatory and oxidative effects of CO poisoning. New methods to directly target the toxic effect of CO, such as CO scavenging agents, are currently under development.

Carbon monoxide (CO) poisoning is common in modern society, resulting in significant morbidity and mortality in the United States annually. Over the past two decades, sufficient information has been published about carbon monoxide poisoning in the medical literature to draw firm conclusions about many aspects of the pathophysiology, diagnosis, and clinical management of the syndrome, along with evidence-based recommendations for optimal clinical practice. This article provides clinical practice guidance to the pulmonary and critical care community regarding the diagnosis, management, and prevention of acute CO poisoning. The article represents the consensus opinion of four recognized content experts in the field. Supporting data were drawn from the published, peer-reviewed literature on CO poisoning, placing emphasis on selecting studies that most closely mirror clinical practice.

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.

Delayed encephalopathy after carbon monoxide poisoning (DEACMP) is the most severe and prevalent neurological sequela associated with carbon monoxide exposure. This study aims to investigate the time-varying characteristics of dynamic brain networks and their topological properties in DEACMP patients using resting-state functional magnetic resonance imaging (rs-fMRI). We conducted Functional MRI scans and clinical assessments for 25 DEACMP patients and 25 healthy controls (HCs). To capture the variability patterns of dynamic functional connectivity (dFC) between the two groups, we employed a sliding time window analysis method. Additionally, theoretical graph analysis was utilized to examine the variations in the topological properties of whole-brain functional networks. We found that DEACMP patients have two dFC states characterized by different connection patterns, State 1 and State2, and there were multiple inter-network and intra-network dynamic interactions in State2.Next, Abnormal dFC indicators were related to the MoCA scores. Finally, the dynamic brain network topological properties were variable. These findings may provide valuable insights into the disruptions in local information transmission and processing functions within the brain’s functional networks in individuals with DEACMP.

Carbon monoxide (CO) poisoning is a common health problem among people in many countries, primarily because of its severe clinical effects and high toxicological morbidity and mortality. Acute brain injury and delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) are the most common neurological complications. This study was performed to assess the efficacy of N-butylphthalide (NBP) and dexamethasone (DXM) combined with hyperbaric oxygen (HBO) in patients with DEACMP. A total of 171 patients with DEACMP were recruited and assigned to the combined therapy group (receiving NBP and DXM 5 mg/day plus HBO therapy) or the control group (HBO therapy as monotherapy). Conventional treatments were provided for all patients. The cognition and movement changes in patients were evaluated by the Mini-Mental State Examination (MMSE), the Montreal Cognitive Assessment (MoCA) scale and the Barthel index of activities of daily living (ADL) before and after the treatment at 1 month, 3 months, and 1 year, respectively. At 1 month, 3 months, and 1 year after the treatment, the MMSE, MoCA and ADL scores were all significantly higher in the combined therapy group than those in the control group. There were no significant alterations in blood glucose, blood lipids, or liver and kidney function during the whole treatment session. Some patients experienced loss of appetite, mild headache and minor skin irritations. However, these patients recovered by themselves and needed no additional medications or special treatment. These results indicated that NBP and DXM combined with HBO for the treatment of DEACMP can significantly improve the cognitive and motor functions of patients and is very safe.

In this study, we analyzed the factors influencing the development of delayed encephalopathy in patients with acute carbon monoxide poisoning (ACOP) (DEACMP) following conventional treatment such as hyperbaric oxygen therapy (HBOT). Between January 2012 and January 2022, we retrospectively analyzed 775 patients with ACOP, who were admitted to the Second Department of Rehabilitation Medicine and received HBOT in the Second Hospital of Hebei Medical University. These patients were divided into the non-DEACMP and DEACMP groups based on their follow-up; we then compared the general data, clinical characteristics, admission examination, and treatment between the two groups to identify risk factors for the development of DEACMP. The DEACMP group comprised of 168 cases, while the non-DEACMP group consisted of 607 cases. Univariate analysis showed that there were 20 possible prognostic factors in the non-DEACMP and DEACMP groups. The results of multivariable regression analyses suggested that the occurrence of DEACMP was significantly correlated with advanced age, the combination of multiple medical histories, the duration of CO exposure, the duration of coma, poisoning degree, the Interval between ACOP and the first HBOT, the total number of HBOTs, and the combination with rehabilitation treatment. DEACMP patients who are older, have more comorbidities, prolonged CO exposure, prolonged coma, severe intoxication, long intervals between ACOP and the first HBOT, fewer HBOT treatments, and who are not treated with a combination of rehabilitative therapies have a poor prognosis.

Carbon monoxide (CO) results from incomplete combustion of carbon-based materials, causing symptoms such as headaches, dizziness, nausea, chest pain, confusion, and, in severe cases, unconsciousness. Normobaric oxygen therapy (NBOT) is the standard therapy, whereas hyperbaric oxygen therapy (HBOT) is recommended in severe cases of organ damage. This study examined the early and late adverse outcomes in patients with severe CO poisoning. This study analyzed severe cases of CO poisoning among patients admitted to the emergency department between January 2020 and May 2022. The demographic, clinical, and laboratory data of symptomatic individuals and those requiring HBOT were examined. The study recorded early outcomes, such as intubation and in-hospital mortality, and late outcomes, such as delayed neurological sequelae and 1-year mortality. Chi-square tests, Spearman's rho correlation tests, and logistic regression analyses were performed to identify factors affecting these outcomes. Patients who received HBOT showed a significant difference in delayed neurological sequelae (DNS) compared to those who received NBOT (p = 0.037). Significant differences were observed in the need for intubation, in-hospital mortality, and 1-year mortality between patients based on COHb levels, but no significant differences were found in DNS. The 1-year mortality probability was significantly influenced by COHb level (odds ratio = 1.159, 95% CI [1.056-1.273]). Patients receiving NBOT had a higher odds ratio for DNS risk than those receiving HBOT (odds ratio = 8.464, 95% [1.755-40.817], p = 0.008). The study showed no differences in intubation, in-hospital mortality, and 1-year mortality rates between the HBOT and NBOT groups. However, significant differences in DNS suggest that treatment modalities have different effects on neurological outcomes. High COHb levels are associated with an increased risk of intubation, and mortality underscores the significance of monitoring COHb levels in clinical evaluations.

To examine trends in the incidence of carbon monoxide poisoning before and after a ban on domestic use of raw coal in Ulaanbaatar, Mongolia. Using injury surveillance data and population estimates, we calculated the incidence per 100 000 person-years of fatal and non-fatal domestic carbon monoxide poisoning before (May 2017 to April 2019) and after (May 2019 to April 2022) the ban in May 2019. We analysed data by age and sex, and compared areas not subjected to the ban with districts where domestic use of raw coal was banned and replaced with refined coal briquettes. We obtained complete data on 2247 people with carbon monoxide poisoning during the study period in a population of around 3 million people. In districts with the ban, there were 33 fatal and 151 non-fatal carbon monoxide poisonings before the ban, and 91 fatal and 1633 non-fatal carbon monoxide poisonings after the ban. The annual incidence of poisoning increased in districts with the ban, from 7.2 and 6.4 per 100 000 person-years in the two 12-month periods before the ban to 38.9, 42.0 and 40.1 per 100 000 in the three 12-month periods after the ban. The incidence of poisoning remained high after the ban, despite efforts to educate the public about the correct use of briquettes and the importance of ventilation. The incidence of carbon monoxide poisoning also increased slightly in areas without the ban. Efforts are needed to investigate heating practices among households using briquettes, and to determine factors causing high carbon monoxide concentrations at home.

Objective To investigate alterations in hippocampal subfields in patients with acute carbon monoxide poisoning (ACMP) and explore their relationship with neurocognitive function. Materials and Methods Forty‐seven ACMP patients and 29 age‐ and sex‐matched healthy controls (HCs) were recruited. All ACMP patients underwent carboxyhemoglobin (COHb) assessment at admission and acquired MRI scans within 3 days post‐exposure. Cognitive functions were assessed using the mini‐mental state examination (MMSE) and Montreal Cognitive Assessment (MoCA), and activities of daily living were evaluated using the Functional Independence Measure (FIM) and Barthel Index (BI). Differences in hippocampal volume between groups were analyzed using Analysis of Covariance (ANCOVA), and correlations with cognitive and functional scores were evaluated. Results After follow‐up, 27.66% (13/47) of ACMP patients developed Delayed Encephalopathy After Carbon Monoxide Poisoning (DEACMP). The COHb concentration was significantly higher in the DEACMP group (median 17.70% vs. 11.95%, z = −2.225, p = 0.026) compared to the Recovery group. The cognitive function scores, delayed memory‐related sub‐items scores derived from cognitive assessments, and activities of daily living scores in the DEACMP group were lower than those in the Recovery group (all p < 0.05). The ACMP group showed significant volume reduction in the bilateral whole hippocampus, cornu ammonis (CA) cornu ammonis 3, CA4, GC.ML.DG, Moleculat_layer, and right subiculum compared to HCs. The right subiculum and right CA4 volumes were smaller in the DEACMP group than in the Recovery group. The ROC curve analysis indicated that the combination of COHb concentration, MoCA, and FIM scores had good predictive value for DEACMP(the area under the ROC curve = 0.887, p < 0001). Correlation analysis showed that MoCA‐delayed recall was positively associated with the volume of the left CA1 subfield (r = 0.357, p = 0.020), and MMSE‐delayed recall was positively associated with the volume of the left presubiculum (r = 0.323, p = 0.037). Conclusion This study is the first to report specific hippocampal subfield alterations in ACMP patients, suggesting their potential as non‐invasive markers of hippocampal injury. The hippocampal subfields may contribute to the development of DEACMP by modulating cognitive processes. These findings may improve understanding of the neurological impact of hypoxic injuries in human subject research. This study investigated the relationship between hippocampal subfield volumes and cognitive impairments in patients with ACMP. We found significant volume reductions in the bilateral CA3, CA4, GC.ML.DG, Moleculat_layer, and right subiculum in ACMP patients. Among ACMP patients, patients who developed DEACMP had smaller volumes in the right CA4 and right subiculum. Specific hippocampal subfields may be involved in the development of DEACMP by potentially modulating cognitive processes.

Aims The objective of this study is to explore the regulatory role of DNA methylation in delayed encephalopathy after carbon monoxide poisoning (DEACMP) and to identify candidate epigenetic biomarkers. Methods In this study, multi‐omics analyses such as methylomics, transcriptomics, pyrophosphate sequencing, qRT‐PCR, immunohistochemistry, and western blotting were utilized to investigate the role of epigenetic regulation and altered gene expression in the pathogenesis of DEACMP. Results Using integrated analysis, we identified 168 differentially methylated CpGs sites, 334 differentially expressed genes, and two differentially methylated and differentially expressed genes (DAB2IP and SMYD3) in the DEACMP group. The pyrosequencing results further revealed hypomethylation of DAB2IP and hypermethylation of SMYD3. Moreover, we verified the upregulation of DAB2IP expression accompanied by the downregulation of SMYD3 expression in the DEACMP rats model. Conclusion This study, based on dysregulated DNA methylation and gene expression profiles, identified and validated two DEACMP‐related genes (DAB2IP and SMYD3) that could serve as epigenetic biomarkers and potential therapeutic targets for DEACMP. By integrating DNA methylation and gene expression from patients with delayed encephalopathy after carbon monoxide poisoning (DEACMP), this study identified DAB2IP and SMYD3 as candidate genes potentially involved in DEACMP pathogenesis. Additionally, further evidence for their potential as DEACMP targets was provided through pyrosequencing and DEACMP rat model.