Edaravone combined with hyperbaric oxygen therapy in delayed encephalopathy after acute carbon monoxide poisoning: A meta-analysis.

BACKGROUND: The use of both edaravone (EDA) and hyperbaric oxygen therapy (HBOT) is increasingly prevalent in the treatment of delayed encephalopathy after carbon monoxide poisoning (DEACMP). This meta-analysis aims to evaluate the efficacy of using EDA and HBOT in combination with HBOT alone in the treatment of DEACMP. METHODS: We searched and included all randomized controlled trials (RCTs) published before November 6, 2023, from 12 Chinese and English databases and clinical trial centers in China and the United States. The main outcome indicator was the total effective rate. The secondary outcome indicators included the Mini-Mental State Examination (MMSE), Montreal Cognitive Assessment (MoCA), National Institutes of Health Stroke Scale (NIHSS), Barthel Index (BI), Hasegawa Dementia Scale (HDS), Fugl-Meyer Assessment (FMA), Superoxide Dismutase (SOD), and Malondialdehyde (MDA). Statistical measures utilized include risk ratios (RR), weighted mean difference (WMD), and 95 % confidence intervals (95 % CI). RESULTS: Thirty studies involving a combined total of 2075 participants were ultimately incorporated. It was observed that the combination of EDA with HBOT for the treatment of DEACMP demonstrated an improvement in the total effective rate (RR: 1.25; 95 % CI: 1.20-1.31; P < 0.01), MMSE (WMD: 3.67; 95 % CI: 2.59-4.76; P < 0.01), MoCA (WMD: 4.38; 95 % CI: 4.00-4.76; P < 0.01), BI (WMD: 10.94; 95 % CI: 5.23-16.66; P < 0.01), HDS (WMD: 6.80; 95 % CI: 4.05-9.55; P < 0.01), FMA (WMD: 8.91; 95 % CI: 7.22-10.60; P < 0.01), SOD (WMD: 18.45; 95 % CI: 16.93-19.98; P < 0.01); and a reduction in NIHSS (WMD: -4.12; 95 % CI: -4.93 to -3.30; P < 0.01) and MDA (WMD: -3.05; 95 % CI: -3.43 to -2.68; P < 0.01). CONCLUSION: Low-quality evidence suggests that for DEACMP, compared to using HBOT alone, the combined use of EDA and HBOT may be associated with better cognition and activity of daily living. In the future, conducting more meticulously designed multicenter and large-sample RCTs to substantiate our conclusions is essential.

Delayed encephalopathy after acute carbon monoxide poisoning: a case study.

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a relatively rare inflammatory-associated neurometabolic complication. In this article, we present a case report of a 50-year-old male patient with a history of carbon monoxide poisoning. This acute poisoning, although successfully controlled during a stay in the intensive care unit of a local hospital, later led to persistent neurological symptoms. The patient was then treated in the inpatient unit of the rehabilitation clinic, where cognitive deterioration began to develop 20 days after admission. Subsequent examination using EEG and magnetic resonance imaging confirmed severe encephalopathy later complicated by SARS-CoV-2 infection with fatal consequences due to bronchopneumonia. Because currently there are no approved guidelines for the management of DEACMP, we briefly discuss the existing challenges for future studies, especially the application of rational immunosuppressive therapy already in the acute treatment phase of CO poisoning, which could prevent the development of a severe form of DEACMP.

Evidence of clinical efficacy and pharmacological mechanism of N-butylphthalide in the treatment of delayed encephalopathy after acute carbon monoxide poisoning.

Objective: Based on network meta-analysis (NMA) and network pharmacology approaches, we explored the clinical efficacy of different regimens, and clarified the pharmacological mechanisms of N-butylphthalide (NBP) in the treatment of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Methods: Firstly, NMA was conducted to obtain the ranking of the efficacy of different regimens for the treatment of DEACMP. Secondly, the drug with a relatively high efficacy ranking was selected and its mechanism of treatment for DEACMP was identified through a network pharmacology analysis. By the use of protein interaction and enrichment analysis, the pharmacological mechanism was predicted, and molecular docking was subsequently carried out to verify the reliability of the results. Results: A total of 17 eligible randomized controlled trials (RCTs) involving 1293 patients and 16 interventions were eventually included in our analysis from NMA. Mesenchymal stem cells (MSCs) + NBP significantly increased mini-mental state examination (MMSE) and Barthel index (BI) scores; NBP + dexamethasone (DXM) was the most effective treatment in improving the activity of daily living (ADL) scores; NBP significantly decreased national institutes of health stroke scale (NIHSS) scores; Xingzhi-Yinao granules (XZYN) had more advantages in improving Montreal cognitive assessment (MoCA) scores, translational direct current stimulation (tDCS) had a significant effect in improving P300 latency and P300 amplitude and Kinnado + Citicoline had the most obvious effect in improving malondialdehyde (MDA). Meanwhile, by network pharmacology analysis, 33 interaction genes between NBP and DEACMP were obtained, and 4 of them were identified as possible key targets in the process of MCODE analysis. 516 Gene ontology (GO) entries and 116 Kyoto Encyclopedia of Gene and Genome (KEGG) entries were achieved by enrichment analysis. Molecular docking showed that NBP had good docking activity with the key targets. Conclusion: The NMA screened for regimens with better efficacy for each outcome indicator in order to provide a reference for clinical treatment. NBP can stably bind ALB, ESR1, EGFR, HSP90AA1, and other targets, and may play a role in neuroprotection for patients with DEACMP by modulating Lipid and atherosclerosis, IL-17 signaling pathway, MAPK signaling pathway, FoxO signaling pathway, PI3K/AKT signaling pathway.

[Research progress on head imaging features of carbon monoxide poisoning and delayed encephalopathy].

Acute carbon monoxide poisoning and its delayed encephalopathy have obvious damage to the central nervous system. There are different neuroimaging changes in different stages of the disease, and they are relatively specific. This article reviews the clinical research progress on the imaging changes of carbon monoxide poisoning and delayed encephalopathy, including computed tomography (CT) , conventional magnetic resonance imaging (MRI) , diffusion weighted imaging (DWI) , diffusion tensor imaging (DTI) , diffusion kurtosis imaging (DKI) , magnetic resonance spectroscopy (MRS) and other imaging changes reflecting the function and metabolic state of the brain tissue.

Correlation Between Rats Hippocampal ATP Content and Delayed Encephalopathy After Acute Carbon Monoxide Poisoning.

Objective: To study the correlation between the adenosine triphosphate (ATP) content in the hippocampus of rats and delayed encephalopathy after acute carbon monoxide (CO) poisoning. Methods: A total of 40 male Wistar rats weighing 180-230g, in accordance with the random number table, were selected and divided into the delayed encephalopathy after acute carbon monoxide poisoning (DEACMP: Rats with cognitive impairment after carbon monoxide poisoning) group (n = 32) and the control group (n = 8). A DEACMP rat model was generated by inhalation of CO. The Morris water maze evaluated the ability to learn and memorize in rats. The changes in neurons in the hippocampus of the rats were observed by hematoxylin-eosin (HE) staining. Lastly, the ATP content in the hippocampus of the rats was measured by high-performance liquid chromatography (HPLC). Results: The ATP content of the experimental group was significantly higher than that of the control group in the hippocampus of the rat model, so the difference was statistically significant (P < 0.05); the intra-group comparison was made for the ATP content in the experimental group, and the difference was statistically significant as group 21d > group 14d > group 7d (P < 0.05); and no significant difference was found between group 21d and group 28d (P > 0.05). Conclusion: The changes in the ATP content in the hippocampus of the rats are correlated with the occurrence of delayed encephalopathy after acute carbon monoxide poisoning; it may take part in the pathogenesis of DEACMP. This offers some elicitation to the prevention and treatment of the disease.

Investigation of the relationship between MBP gene polymorphisms and delayed encephalopathy after acute carbon monoxide poisoning.

Increasing evidence reveals that delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) results from the combined effects of environmental and genetic factors. The main pathological feature of DEACMP was generalized demyelination of cerebral white matter. Myelin basic protein (MBP) levels in cerebrospinal fluid (CSF) and serum samples from DEACMP patients were elevated. This study investigated the association of MBP single nucleotide polymorphisms(SNPs) (rs470555, rs470724, rs4890785, rs595997, rs76452994, and rs921336) with DEACMP. We genotyped 416 DEACMP patients and 785 age, educational level, and sex-matched ACMP patients for rs470555, rs470724, rs4890785, rs595997, rs76452994, and rs921336 SNPs using the Agena MassArray. There were no significant differences in the allele frequency distribution, four genetic models, and genotype distributions between the DEACMP and ACMP groups for rs470555, rs470724, rs4890785, and rs595997. However, significant differences were observed for rs76452994 and rs921336. This study revealed that the MBP polymorphisms, rs470555, rs470724, rs4890785, and rs595997, were not associated with DEACMP. Based on the codominant, dominant, and overdominant genetic inheritability patterns, the MBP rs76452994 and rs921366 polymorphisms were associated with DEACMP. Furthermore, the G allele of rs76452994 and T allele of rs921336 could lead to higher DEACMP risk.

Research progress on head imaging features of carbon monoxide poisoning and delayed encephalopathy / 中华劳动卫生职业病杂志

Acute carbon monoxide poisoning and its delayed encephalopathy have obvious damage to the central nervous system. There are different neuroimaging changes in different stages of the disease, and they are relatively specific. This article reviews the clinical research progress on the imaging changes of carbon monoxide poisoning and delayed encephalopathy, including computed tomography (CT) , conventional magnetic resonance imaging (MRI) , diffusion weighted imaging (DWI) , diffusion tensor imaging (DTI) , diffusion kurtosis imaging (DKI) , magnetic resonance spectroscopy (MRS) and other imaging changes reflecting the function and metabolic state of the brain tissue.

Effect of hyperbaric oxygen on symptoms of dementia in patients with delayed encephalopathy after acute carbon monoxide poisoning. / é«˜åŽ‹æ°§å¯¹æ€¥æ€§ä¸€æ°§åŒ–ç¢³ä¸­æ¯’è¿Ÿå‘æ€§è„‘ç— æ‚£è€ ç—´å‘†ç—‡çŠ¶çš„å½±å“ï¼ˆè‹±æ–‡ï¼‰.

OBJECTIVES: Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is the most severe complication of carbon monoxide poisoning, which seriously endangers patients' quality of life. This study aims to investigate the efficacy of hyperbaric oxygen (HBO2) on improving dementia symptoms in patients with DEACMP. METHODS: A retrospective analysis was performed on DEACMP patients, who visited Xiangya Hospital, Central South University from June 2014 to June 2020. Among them, patients who received conventional drug treatment combined with HBO2 treatment were included in an HBO2 group, while those who only received conventional drug treatment were included in a control group. HBO2 was administered once daily. Patients in the HBO2 group received 6 courses of treatment, with each course consisting of 10 sessions. The Hasegawa Dementia Scale (HDS) was used to diagnose dementia, and the Clinical Dementia Rating (CDR) was used to grade the severity of dementia for DEACMP. The Alzheimer's Disease Assessment Scale-Cognitive Section (ADAS-Cog), the Functional Activities Questionnaire (FAQ), the Neuropsychiatric Inventory (NPI), and the Clinician's Interview-Based Impression of Change-Plus Caregiver Input (CIBIC-Plus) were performed to assess cognitive function, ability to perform activities of daily living (ADL), behavioral and psychological symptoms, and overall function. The study further analyzed the results of objective examinations related to patients' dementia symptoms, including magnetic resonance imaging detection of white matter lesions and abnormal electroencephalogram (EEG). The changes of the above indicators before and after treatment, as well as the differences between the 2 groups after treatment were compared. RESULTS: There was no significant difference in the HDS score and CDR grading between the 2 groups before treatment (both P>0.05). After treatment, the score of ADAS-Cog, FAQ, NPI, and CIBIC Plus grading of the 2 groups were significantly improved, and the improvement of the above indicators in the HBO2 group was greater than that in the control group (all P<0.05). The effective rate of the HBO2 group in treating DEACMP was significantly higher than that of the control group (89.47% vs 65.87%, P<0.05). The objective examination results (white matter lesions and abnormal EEG) showed that the recovery of patients in the HBO2 group was better than that in the control group. CONCLUSIONS: Hyperbaric oxygen can significantly relieve the symptoms of dementia in patients with DEACMP.

Correlation analysis of apparent diffusion coefficient combined with C-reactive protein on delayed encephalopathy caused by carbon monoxide poisoning / 中华急诊医学杂志

Objective:To investigate the Correlation between ADC combined with serum C-reactive protein (CRP) and delayed encephalopathy after carbon monoxide poisoning (DEACMP), It provides scientific basis for early prediction of DEACMP.Methods:According to the design principle of case-control study, the data of acute carbon monoxide poisoning (ACOP) patients admitted to Shandong Provincial Hospital from December 2017 to December 2021 were retrospectively selected. Among them, patients with DEACMP were selected as the case group, without DEACMP were used as the control group. Univariate and multivariate analyses were performed on the two groups. Receiver operating characteristic curve (ROC) was used to evaluate the diagnostic efficacy of ADC combined with CRP as a combined predictor for disease.Results:A total of 89 patients with ACOP were included, including 33 patients with DEACMP and 56 patients without DEACMP. There were no significant differences in gender, age, smoking, drinking, and underlying diseases (hypertension, coronary heart disease) between groups ( P>0.05). Logistic regression analysis showed that white blood cell count (WBC) ( OR=1.64, 95% CI: 1.19-2.26, P=0.003), CRP ( OR=1.22, 95% CI: 1.03-1.45, P=0.019) and ADC value of central semiovale white matter ( OR=0.99, 95% CI: 0.98-1.00, P=0.010) were associated with DEACMP in patients with ACOP. The ROC curve results showed that the area under the ROC of ADC combined with CRP in the center of semiovale was 0.765 (95% CI: 0.656-0.845), the specificity was 87.9%, the sensitivity was 23.2%, and the cut-off value was 3.5°. Conclusions:WBC, CRP and ADC value of central semiovale are independent factors for DEACMP. ADC value of central semiovale combined with CRP has more clinical value in the early diagnosis of DEACMP. For ACOP patients with DEACMP triggering factors, the diagnosis and treatment awareness of early screening of brain magnetic resonance imaging should be strengthened to avoid DEACMP.

Protective effect and mechanism of hyperbaric oxygen on delayed encephalopathy after carbon monoxide poisoning via the mitochondrial pathway in mice / 中华急诊医学杂志

Objective:To explore the protective effect and underlying mechanism of hyperbaric oxygen (HBO) on delayed encephalopathy after carbon monoxide poisoning (DEACMP) in mice.Methods:Totally 225 adult male Kunming mice were selected to establish CO poisoning model via intraperitoneal injection carbon monoxide (CO), and were randomly divided into the air control group, CO poisoning group, and HBO group. Each group was further divided into five time points group, that was 1, 3, 7, 14 and 21 d. The mice in the air control group were injected intraperitoneally with the same amount of air, and the HBO group received HBO treatment at the same time every day. DEACMP mice model was screened by behaviors using the open field test, new object recognition test and nesting test, and the content of myelin basic protein (MBP) were assayed. The mouse brain tissue and mitochondrial were prepared and malonialdehyde (MDA) and adenosine triphosphate (ATP) content were measured with ultraviolet spectrophotometer. MBP content in brain tissue and cytochrome C (CytC) content in the mitochondrial were measured by ELISA. The mitochondria membrane potential (MMP) was measured by flow cytometry.Results:Compared with the air control group, the content of carboxyhemoglobin (COHB) in blood increased significantly and the content of MBP in brain tissue decreased significantly in CO poisoning mice. CO poisoning mice showed motor ability and cognitive dysfunction. Compared with the air control group, the contents of MMP, CytC and ATP were significantly decreased ( P<0.01) in the CO poisoning group; while the MDA content was significantly increased ( P<0.01). Compared with the CO poisoning group, mice behaviors were improved significantly ( P<0.05), the content of MBP, MMP, CytC and ATP were increased ( P<0.05), while the MDA content decreased significantly ( P<0.01) in the HBO group. Conclusions:The abnormal mitochondrial function might be closely related to the occurrence and development of DEACMP, and HBO therapy plays an effective role in preventing and treating the DEACMP mice model via the mitochondrial pathway.

Development of a Nomogram Based on Diffusion-Weighted Imaging and Clinical Information to Predict Delayed Encephalopathy after Acute Carbon Monoxide Poisoning.

BACKGROUND: Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a severe complication that can arise from acute carbon monoxide poisoning (ACOP). This study aims to identify the independent risk factors associated with DEACMP and to develop a nomogram to predict the probability of developing DEACMP. METHODS: The data of patients diagnosed with ACOP between September 2015 and June 2021 were analyzed retrospectively. The patients were divided into the two groups: the DEACMP group and the non-DEACMP group. Univariate analysis and multivariate logistic regression analysis were conducted to identify the independent risk factors for DEACMP. Subsequently, a nomogram was constructed to predict the probability of DEACMP. RESULTS: The study included 122 patients, out of whom 30 (24.6%) developed DEACMP. The multivariate logistic regression analysis revealed that acute high-signal lesions on diffusion-weighted imaging (DWI), duration of carbon monoxide (CO) exposure, and Glasgow Coma Scale (GCS) score were independent risk factors for DEACMP (Odds Ratio = 6.230, 1.323, 0.714, p < 0.05). Based on these indicators, a predictive nomogram was constructed. CONCLUSIONS: This study constructed a nomogram for predicting DEACMP using high-signal lesions on DWI and clinical indicators. The nomogram may serve as a dependable tool to differentiate high-risk patients and enable the provision of personalized treatment to lower the incidence of DEACMP.

Prognostic factors of hyperbaric oxygen therapy for patients with delayed encephalopathy after acute carbon monoxide poisoning.

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is a disease with an incomplete pathological mechanism, long treatment time, and uncertain factors affecting the therapeutic effect. This study explored prognostic factors for DEACMP patients treated with hyperbaric oxygen therapy (HBOT) in 15 hospitals in China. The findings might provide a theoretical basis for further improving the prognosis of DEACMP patients. In this study, data from 330 patients with DEACMP who were admitted to HBOT centers of 15 hospitals in Hunan Province (China) from June 2015 to June 2020 were retrospectively analyzed, and their medical records related to disease prognosis were collected and followed up by telephone. Univariate and multivariate analyses were used to identify independent risk factors for the prognosis of DEACMP patients after HBOT. Univariate analysis revealed 11 possible prognostic factors. Consistent with univariate analysis, multivariate analysis found that underlying diseases (Odds radio(OR) = 2.886, P = 0.048), hypermyotonia (OR = 5.2558, P = 0.008), and HBOT pressure no less Than 2.3 atm absolute (ATA) ((OR = 7.812, P = 0.004) were identified as independent prognostic factors among 20 variables for poor prognosis of DEACMP patients treated with HBOT in the study. This multicenter retrospective analysis revealed that the adverse prognostic markers for DEACMP patients treated with HBOT might be underlying diseases, hypermyotonia, and an HBOT pressure of 2.3 ATA or higher.

[A suspected case of delayed encephalopathy after acute hydrogen sulfide poisoning].

The main component of the gas in the fish storage tank is hydrogen sulfide. Hydrogen sulfide poisoning is a common occupational chemical poisoning among fishermen in summer, and acute hydrogen sulfide poisoning can manifest as toxic encephalopathy. This paper analyzes a patient with delayed encephalopathy suspected of acute hydrogen sulfide poisoning. The patient was unconscious for 18 days after waking up for 5 days after acute hydrogen sulfide poisoning. After waking up again, there were symptoms such as decreased limb muscle strength, ataxia, swallowing, dysarthria, and the clinical characteristics were significantly different from those of delayed encephalopathy caused by acute carbon monoxide poisoning, such as decreased cognitive function and damage to extrapyramidal system.

[Research progress on the mechanisms of delayed encephalopathy in acute carbon monoxide poisoning].

In our country, there are a large number of carbon monoxide poisoning patients every winter. 10% to 30% of patients with acute carbon monoxide poisoning develop acute carbon monoxide poisoning delayed encephalopathy after a "false recovery period" of about 2 to 60 days. The morbidity and mortality rates of the disease are extremely high, but there is still no effective treatment for this condition. The pathogenesis of the disease is complex, and there is no clear conclusion yet. After consulting a large number of recent relevant literatures, this article reviews the main research results of the pathogenesis of the disease so far, with an aim to facilitate its early clinical diagnosis and correct treatment.

LncRNA CRNDE Deteriorates Delayed Encephalopathy After Acute Carbon Monoxide Poisoning to Inactivate AKT/GSK3ß/ß-catenin Pathway via miR-212-5p.

Delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) is the most serious sequel of acute CO poisoning, with structure or function injury of the brain. LncRNA colorectal neoplasia differentially expressed (CRNDE) aberrant expression was involved in nerve cell injury; however, the mechanism of CRNDE in DEACMP remains elusive. CO poisoning model of Sprague-Dawley rats was established. Neurological function was measured by Morris water maze (MWM) testing. Histopathological condition of brain and hippocampus tissues was observed by hematoxylin and eosin (H&E), Nissl, and TUNEL staining. Pro-inflammatory cytokine levels were evaluated by enzyme-linked immunosorbent assay (ELISA). Oxidative damage and apoptosis markers were determined by related detection assays. Cell apoptosis were evaluated by flow cytometry analysis. Luciferase report and RNA immunoprecipitation (RIP) assays were employed to identify the binding relationship of CRNDE and miR-212-5p. CRNDE was significantly increased in CO poisoning animal model and oxygen-glucose deprivation (OGD) group, while that of miR-212-5p was decreased. CRNDE knockdown repressed the histopathological damage and apoptosis of brain and hippocampus tissues. Besides, CRNDE suppressed the AKT/GSK3ß/ß-catenin signaling pathway via targeting miR-212-5p. Furthermore, the protective effects of CRNDE silencing on brain tissue injury and apoptosis and AKT/GSK3ß/ß-catenin signaling pathway were reversed by inhibition of miR-212-5p in CO poisoning model. Collectively, CRNDE, serving as a sponge of miR-212-5p, aggravated the injury and apoptosis of brain and hippocampus tissues through regulating AKT/GSK3ß/ß-catenin signaling pathway under the CO-poisoning and OGD-treated model, suggesting a selected therapeutic target of DEACMP.

Effect of Recombinant Human Brain Natriuretic Peptide on Acute Carbon Monoxide Poisoning Complicated with Heart Failure with Reduced Ejection Fraction.

This paper aims to observe the effect of recombinant human brain natriuretic peptide (rhBNP) on treatment of acute carbon monoxide poisoning (ACMP) complicated with heart failure with reduced ejection fraction (HFREF).A total of 103 patients with ACMP complicated with HFREF admitted to our department from October 2016 to March 2020 were observed. Patients were divided into control group (50 cases) and experimental group (53 cases). The control group was given diuretic, vasodilator, and digitalis treatment, and the experimental group was supplemented with rhBNP treatment based on the control group. Patients' general information was collected. The levels of myocardial injury-associated indicators of patients were detected at and after admission.No significant differences were observed in the general data of patients compared with control group. The acute physiology and chronic health enquiry II score of patients was positively correlated with left ventricular ejection fraction (LVEF). At admission, the levels of myocardial injury indicators, N-terminal B-type brain natriuretic peptide, and cardiac ultrasound indexes had no significant difference between the control group and experimental group. However, after admission, the LVEF and stroke output levels were elevated, while the other indicators were all decreased compared with the control group.The rhBNP exerts a protective effect on ACMP-induced cardiomyocyte injury to improve cardiac function, shorten the length of hospital stay, and reduce the incidence and mortality of delayed encephalopathy after carbon monoxide poisoning.

Relationship between inducible nitric oxide synthase and delayed encephalopathy in carbon monoxide poisoning / 中华急诊医学杂志

Objective:To observe the relationship between inducible carbon monoxide synthase (iNOS) and delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), and explore its mechanism of action in DEACMP.Methods:This study was designed as prospective cohort study. Patients with acute carbon monoxide poisoning who met the diagnostic criteria and were admitted to Emergency Intensive Care Unit(EICU) of our hospital from June 2019 to June 2021 were selected as subjects. Patients were divided into the DEACMP group and non-DEACMP group according to the occurrence of DEACMP. Serum samples were collected on the first 24 h after admission and on day 7 and 14 after admission, and the serum nitric oxide (NO), neuronal nitric oxide synthase (nNOS), inducible carbon monoxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS) level were measured by enzyme-linked immunosorbent assay. The generalized estimating equation was used to estimate the difference of NO, nNOS, iNOS and eNOS between DEACMP and non-DEACMP patients.Results:A total of 78 patients with carbon monoxide poisoning were included in our study finally, including 49 (62.82%) males and 29 (37.18%) females, with an average age of (53.96±14.95) years, 20 (25.64%) patients with DEACMP, and 1 (1.28%) death. Univariate analysis showed that patients with DEACMP had an average increase of 3 h (95% CI: 1.00, 5.00) in carbon monoxide exposure time and a 5-point decrease in GCS score (95% CI: 1.00, 6.00) than the patients without DEACMP, and the proportion of patients with severe carbon monoxide poisoning in the DEACMP group was higher than that of the non-DEACMP group (90.00% vs. 32.76%). According to the analysis of generalized estimation equation, on day 7 and 14 after admission, Compared with non-DEACMP patients, neither by performing unadjusted nor adjusted analysis with the iNOS of DEACMP patients was significantly higher than that in non-DEACMP patients regardless of whether exposure time, GCS score, coma time or severity of carbon monoxide poisoning were adjusted or not ( P <0.01 or P <0.05). Except for the level of nNOS in the GEE model adjusted with carbon monoxide exposure time, the levels of NO, nNOS and eNOS showed no significant difference between DEACMP and non-DEACMP patients ( P >0.05). Conclusions:The expression of iNOS level is increased in DEACMP patients, and its continuous expression may be involved in the pathogenesis of DEACMP.

The Effect of Adding Transcranial Direct Current Stimulation to Hyperbaric Oxygen Therapy in Patients With Delayed Encephalopathy After Carbon Monoxide Poisoning: A Randomised Controlled Trial.

Objective: To investigate the effect of transcranial direct current stimulation (tDCS) combined with hyperbaric oxygen therapy (HBOT) in patients with delayed encephalopathy after carbon monoxide poisoning (DEACMP). Design: A parallel-group, open-label randomised controlled study. Setting: Hyperbaric Oxygen Therapy Room of the Second Hospital of Hebei Medical University. Subjects: A total of 40 patients were recruited for the current study. Patients were randomly divided into a treatment group and a control group (20 cases/group). Interventions: Control group: conventional, individualised rehabilitation therapy. Treatment group: conventional, individualised rehabilitation therapy and tDCS. Main Measures: cognitive function of patients, the Barthel Index (BI). Results: After treatment, significantly higher MMSE and BI scores, as well as a greater reduction in P300 latency and an increase in P300 amplitude, were observed in the treatment group compared to the control group (MMSE: 13 ± 7 vs. 9 ± 5; P300 latency: 342 ± 29 vs. 363 ± 17 ms; P300 amplitude: 7.0 ± 3.3 vs. 5.1 ± 2.7 µV; all P < 0.05). In both groups, however, MMSE and BI scores, in addition to P300 amplitude, were significantly improved; in contrast, there was a decrease in P300 latency in both groups after treatment compared to before treatment (all P < 0.05). Conclusion: Combined with HBOT, tDCS can help improve cognitive function and ADL in patients with DEACMP. This combination therapy might be a helpful method to enhance the recovery of patients with DEACMP.

[The predictive value of low T3 syndrome for delayed encephalopathy caused by severe acute carbon monoxide poisoning].

Objective: To explore the predictive value of low T3 syndrome (LT3S) for patients with delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) . Methods: In May 2020, 137 severe acute carben monoxide poisoning (SACMP) patients were selected from Harrison International Peace Hospital Affiliated to Hebei Medical University from January 2019 to January 2020 as subjects. Blood samples were taken after admission to test thyroid function. Followed up for 60 d, the patients were divided into DEACMP group (45 cases) and non DEACMP group (92 cases) according to their prognosis. Clinical data of patients in two groups were collected and compared. The Cox regression with multiple independent variables was used to analyze the independent risk factors of DEACMP. Pearson correlation analysis was used to evaluate the correlation between totall triiodochyronine (TT3) level and Acute Physiology and Chronic Health Evaluation (APACHE) Ⅱ score. The receiver operating characteristic (ROC) curve of TT3 and APACHE Ⅱ scores for predicting DEACMP were drawn. Results: Compared with non DEACMP group, the age, APACHE II score, LT3S rate and diabetes prevalence in DEACMP group were higher, and the Glasgow coma scale (GCS) score was lower (P<0.05) . Cox regression analysis showed that age, APACHEⅡ score and LT3S were independent risk factors of DEACMP in patients with SACMP (OR=1.040, 95%CI:1.005-1.077; OR=1.070, 95%CI: 1.002-1.143; OR=4.210, 95%CI: 1.707-10.379; P<0.05) . Pearson correlation analysis showed that TT3 level was negatively correlated with APACHE Ⅱ score (r=-0.397, P=0.000) . ROC curve showed that the cut-off value of TT3 level for DEACMP prediction was 1.078 nmol/L, the area under curve (AUC) was 0.755, the sensitivity was 82.6%, and the specificity was 73.3%. The cut-off value of the APACHE Ⅱ score for predicting DEACMP was 16, and the AUC was 0.725, sensitivity was 93.3%, and specificity was 60.9%. Conclusion: This study showed that LT3S minght be an independent predictor of DEACMP in patients with SACMP. Thyroid function is closely related to the severity of SACMP patients.

The efficacy of Rhodiola Rosea based on DTI image Segmentation Algorithm for patients with delayed Encephalopathy caused by CO poisoning.

OBJECTIVES: By using DTI image segmentation algorithm investigate the effect of large plants Rhodiola injection on myocardial injury in patients with acute severe CO poisoning (ACOP), and to explore the clinical and CT delayed encephalopathy after ACOP. METHODS: Seventy-two ACOP patients were randomly divided into control and observation group, 36 cases in each group from December 2015 - December 2017. The control group received hyperbaric oxygen, mannitol, dexamethasone, citicoline injection, gangliosides, dracone; observation group were large strain Rhodiola injection treatment group based on the once daily for two weeks of continuous treatment. The head CT, head MRI results were analyzed retrospectively. RESULTS: (1) hsCRP and ET-1 in the observation group were significantly lower than those in the control group, and VEGF was significantly higher than that in the control group (P<0.01). No, NOS, and iNOS were significantly lower than those of the control group (P<0.01); (2) CT images of 16 cases showed bilateral symmetrical fusion lesions with blurred edges, low density, and oval center around the ventricle; (3) MRI showed that the lesion was located in the cerebral cortex, white matter lateral ventricle and/or basal ganglia in 12 cases. CONCLUSION: Rhodiola can reduce myocardial vascular endothelial cell injury, improve cardiac function, and protect the damaged myocardium. Meanwhile, after acute CO poisoning delayed encephalopathy early for CT and MRI examination facilitate analysis and prognosis of the disease.