Acute Carbon Monoxide Poisoning Research Articles

A case of extreme carboxyhaemoglominemia due to vaping

Acute carbon monoxide (CO) poisoning is known to cause neurological, metabolic and cardiorespiratory sequalae. However, data on chronic CO exposure are scant, particularly in the context of vaping, which recent literature suggests may be a greater source of CO than tobacco cigarette smoking. During a series of admissions at the time of vaping, our patient repeatedly presented with significant CO poisoning and developed pulmonary arterial hypertension with resultant high‐output right heart failure. On each occasion, our patient's levels of carboxyhaemoglobin were both higher and took longer to resolve than 12 smokers who underwent arterial blood gas testing at two time points. Our observation may reveal an association between vaping, chronic carboxyhaemoglobinemia and the development of cardiorespiratory disease. Thus, further studies into the safety of vaping and chronic CO exposure are urged.

Incidence, timing, location, risk factors, and nomogram of lower extremity deep venous thrombosis after acutecarbon monoxide poisoning.

Data on lower extremity deep venous thrombosis (DVT) following acute carbon monoxide (CO) poisoning are lacking. This study aimed to identify the incidence rate, timing, locations, risk factors, and nomogram of lower extremity DVT after acute CO poisoning. A total of 203 patients with acute CO poisoning from October 2019 to April 2021 were included in this retrospective study. Multivariate logistic regression analysis was performed to identify the independent risk factors associated with lower extremity DVT. Nomogram was drawn and area under the curve (AUC) was calculated to predict lower extremity DVT. Overall, 14.3% (29/203) had lower extremity DVT, with incidence rates of 2.5% (5/203) for proximal DVT and 11.8% (24/203) for distal DVT. The lower extremity DVTs involved intermuscular vein in 28 patients, popliteal vein in 5 patients, and posterior tibial vein in 3 patients. The mean time from end of exposure to diagnosis of lower extremity DVT was 1.24days. Among 29 lower extremity DVT cases, 6 (23.1%) DVT cases had thrombolysis. Multivariate logistic regression analysis revealed that long coma duration (P < 0.001) and high D-dimer levels (P < 0.001) were significantly associated with lower extremity DVT. The discrimination of nomogram was good with AUC of 0.93 (95% CI, 0.89-0.98). Clinicians should be aware of and concerned with lower extremity DVT after acute CO poisoning, especially in patientswith long coma duration and high D-dimer levels.

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.

Application value of BIS and S100β combined with Copeptin in patients with acute severe carbon monoxide poisoning

Objective: To explore the application value of bispectral index(BIS) , specific protein 100β(S100β) combined with Copeptinin patients with acute severe carbon monoxide poisoning (ASCMP). Methods: A total of 256 patients with acute carbon monoxide poisoning admitted to Hengshui People's Hospital from June 2018 to June 2020 were collected, and they were divided into 30 mild cases, 40 moderate cases and 186 severe cases according to the degree of poisoning. Among them, patients with severe carbon monoxide poisoning were divided into a poor prognosis group (20 cases) and a good prognosis group (166 cases) according to whether adverse events occurred. The changes of creatine kinase isoenzyme (CK-MB) , N-terminal precursor B-type brain natriuretic peptide (NT-proBNP) , BIS, S100β, and Copeptin in poisoned patients were measured. Logistic regression analysis and receiver operating characteristic (ROC) curve were used to evaluate the significance of relevant indicators for ASCMP patients. Results: Compared with the mild-to-moderate group, CK-MB, NT-proBNP, S100β, Copeptin increased, and BIS value decreased in the severe group (P< 0.05). 24 hours after admission, compared with the good prognosis group, CK-MB, NT-proBNP, S100β, Copeptin in the poor prognosis group increased, and the BIS value decreased (P<0.05). In the poor prognosis group, CK-MB, NT-proBNP, S100β, and Copeptin at 72 hours after admission were all lower than those at 24 hours after admission, and the BIS value was higher than that at 24 hours after admission (P<0.05). Logistic regression analysis showed that ASCMP patients with increased S100β, Copeptin, and decreased BIS values had an increased risk of adverse events (P<0.05). The ROC curve showed that the area under the curve of the combined detection of BIS, S100β and Copeptin was 0.859, which had a great predictive value for the prognosis of ASCMP patients. Conclusion: BIS, S100β combined with Copeptin detection is of great value for early assessment of ASCMP disease and prognosis prediction.

Carbon Monoxide (CO), Nitric Oxide, and Hydrogen Sulfide Signaling During Acute CO Poisoning.

Major toxic effects of acute carbon monoxide (CO) poisoning result from increases in reactive oxygen species (ROS) and reactive nitrogen species (RNS) producing oxidative stress. The importance of altered nitric oxide (NO) signaling in evoking increases in RNS during CO poisoning has been established. Although there is extensive literature describing NO and hydrogen sulfide (H2S) signaling in different types of cells under normal conditions, how CO poisoning-evoked deregulation of additional NO signaling pathways and H2S signaling pathways could result in cell injury has not been previously considered in detail. The goal of this article was to do this. The approach was to use published data to describe signaling pathways driven by CO bonding to different ferroproteins and then to collate data that describe NO and H2S signaling pathways that could interact with CO signaling pathways and be important during CO poisoning. Arteriolar smooth muscle cells—endothelial cells located in the coronary and some cerebral circulations—were used as a model to illustrate major signaling pathways driven by CO bonding to different ferroproteins. The results were consistent with the concept that multiple deregulated and interacting NO and H2S signaling pathways can be involved in producing cell injury evoked during acute CO poisoning and that these pathways interact with CO signaling pathways.

Early neuroimaging and delayed neurological sequelae in carbon monoxide poisoning: a systematic review and meta-analysis

We aimed to assess the evidence regarding the usefulness of brain imaging as a diagnostic tool for delayed neurological sequelae (DNS) in patients with acute carbon monoxide poisoning (COP). Observational studies that included adult patients with COP and DNS were retrieved from Embase, MEDLINE, and Cochrane Library databases in December 2020 and pooled using a random-effects model. Seventeen studies were systematically reviewed. Eight and seven studies on magnetic resonance imaging (MRI) and computed tomography (CT), respectively, underwent meta-analysis. The pooled sensitivity and specificity of MRI for diagnosis of DNS were 70.9% (95% confidence interval [CI] 64.8–76.3%, I2 = 0%) and 84.2% (95% CI 80.1–87.6%, I2 = 63%), respectively. The pooled sensitivity and specificity of CT were 72.9% (95% CI 62.5–81.3%, I2 = 8%) and 78.2% (95% CI 74.4–87.1%, I2 = 91%), respectively. The areas under the curve for MRI and CT were 0.81 (standard error, 0.08; Q* = 0.74) and 0.80 (standard error, 0.05, Q* = 0.74), respectively. The results indicate that detecting abnormal brain lesions using MRI or CT may assist in diagnosing DNS in acute COP patients.

Predicting scale of delayed neuropsychiatric sequelae in patients with acute carbon monoxide poisoning: A retrospective study.

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.

Neurological sequelae in acute carbon monoxide poisoning: Aprospective observational study with MRI data.

Acute carbon monoxide (CO) poisoning survivors may experience persistent neurological sequelae (PNS) and delayed neurological sequelae (DNS). This study evaluated the clinical features, laboratory results, acute brain lesions (ABLs) on diffusion-weighted imaging (DWI) at presentation, and long-term outcomes and explored differences between patients with PNS and DNS. The study included 443 patients who had experienced CO poisoning, underwent DWI and completed 1-year follow-ups. The demographics, comorbidities, symptomatology, laboratory results, ABLs on DWI at presentation, and long-term outcomes were compared between patients with PNS and those with DNS. The 42 (9.5%) and 96 (21.7%) patients with PNS and DNS, respectively, showed no significant differences in demographics, duration of CO exposure, initial conscious level, symptomatology, and laboratory results. ABLs on DWI were observed in 33 patients (33/42) with PNS and 62 patients (62/96) with DNS. The most common region of ABLs was the globus pallidus (60.6% and 56.6% in PNS and DNS, respectively). The proportion of ABLs present and lesion distribution did not differ significantly between the two groups. At 1year, a significantly higher proportion of patients in the PNS group showed a good outcome (defined as modified Rankin Scale [mRS] scores of 0-2, 81%) compared with the DNS group (81% vs. 56.3%, p=.047). Demographics, clinical features, laboratory results, and acute brain lesions on MRI at presentation did not differ between the PNS and DNS groups. However, the long-term outcome of PNS was better than that of DNS.

The Relationship between Cadherin Polymorphisms and the Risk of Delayed Encephalopathy after Acute Carbon Monoxide Poisoning in the Chinese Han Population.

Objective The purpose of this study was to analyze the relationship between cadherin gene single-nucleotide polymorphisms (SNPs) and the risk of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP). Materials and Methods A total of 416 patients with DEACMP and 754 patients with acute carbon monoxide poisoning (ACMP) were recruited. We used the Sequenom MassARRAY® system to detect cadherin gene SNPs related to DEACMP. Using different genetic analysis models, we evaluated the relationship between the cadherin gene polymorphisms and risk of DEACMP. Results We found that rs1944294 in the N-cadherin (CDH2) gene showed significant differences in genotype frequencies between the two groups under codominant and dominant inheritance models. Similarly, rs2513796 in the cadherin-17 (CDH17) gene showed significant differences under the codominant, dominant, and overdominant genetic models. And the T allele frequency of rs1944294 in the DEACMP group was significantly higher than that in the ACMP group (P = 0.023). Conclusions Cadherin gene SNPs (rs1944294, rs2513796) are associated with an increased risk of DEACMP in the Chinese population.

Effect of early intervention on short-term prognosis of patients with myocardial injury induced by acute carbon monoxide poisoning.

AimThis study aimed to investigate the effect of early intervention on the short‐term prognosis of patients with myocardial injury induced by acute carbon monoxide poisoning (ACOP).Methods and resultsWe performed a retrospective cohort study of 139 patients admitted to the hospital for ACOP‐induced acute toxic cardiopathy. Compared with the mild and moderate toxic cardiopathy group, the severe toxic cardiopathy group has significantly increased coma time, acute physiology and chronic health status (APACHE) II score, and the length of hospital stay and significantly reduced proportion of patients with immediate endotracheal intubation and early admission to intensive care unit (ICU) (all P < 0.05). The cardiac troponin I (cTnI) levels and corrected QT dispersion (QTcd) duration in three patient groups were significantly higher (all P < 0.05) than those in the control group, with the highest in the severely toxic heart disease group. Serum cTnI level and QTcd duration were two independent predictors of myocardial injury in ACOP patients. There was a positive correlation between the APACHE II score and serum cTnI level/QTcd duration at admission. The sensitivities of cTnI and QTcd at admission to diagnose serious cardiovascular events were 78.6% and 85.7%, respectively, and the specificities were both 75%.ConclusionsAcute carbon monoxide poisoning patients with myocardial injury need to be admitted to the hospital as early as possible. For patients with severe hypoxia, an artificial airway should be established as early as possible, and patients should be admitted to the monitoring ward to stabilize their condition at the early stage of poisoning. Meanwhile, changes in QTcd, serum cTnI, and creatine kinase‐MB (CK‐MB) should be closely observed.

Inhibition of ROCK2 kinase activity improved behavioral deficits and reduced neuron damage in a DEACMP rat model

The main pathological changes that occur in delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) are extensive demyelination of brain white matter and neuron damage. Previous studies suggested that demyelination and neuron injury are related to activating the Rho/ROCK signaling pathway. Inhibition of the Rho/ROCK signaling pathway can alleviate neuron injury and promote myelin repair. This study utilized a DEACMP model in which rats were prepared by space injection of CO gas intraperitoneally (CO group), and the association between the Rho/ROCK signaling pathway and DEACMP was investigated. The ROCK2 kinase inhibitor Y-27632 was used to prevent the effects of the DEACMP model to elucidate its protective mechanism. The results demonstrated that the cognitive and motor functions were significantly impaired, and the GFAP, NSE, RhoA, and ROCK2 protein levels were significantly increased in the CO group within three weeks after the model was established. After Y-27632 intervention, the cognitive and motor functions of the CO+Y-27632 group were significantly improved within three weeks after the model was established. In the CO+Y-27632 group, the RhoA, ROCK2, GFAP, and NSE (indicating neuron injury) protein levels decreased significantly, and the MBP protein levels (indicating myelin repair) increased significantly within three weeks after the model was established. These results suggested that the pathogenesis of DEACMP was associated with activation of the Rho/ROCK pathway and that Y-27632 inhibited ROCK2 kinase activity in the CO exposed rats, resulting in improved behavioral deficits, reduced neuron damage, and promotion of myelin repair. Therefore, Y-27632 might be a potentially effective drug for the treatment of DEACMP-induced brain damage.

Effect of Dexamethasone Combined with Ganglioside on Acute Carbon Monoxide Poisoning and its Influence on Cognitive Function

Effect of Dexamethasone Combined with Ganglioside on Acute Carbon Monoxide Poisoning and its Influence on Cognitive Function

Evaluation of Various Scoring Systems in Prediction of Acute Carbon Monoxide Poisoning Outcome

Evaluation of Various Scoring Systems in Prediction of Acute Carbon Monoxide Poisoning Outcome

Case Report of Central Delayed Encephalopathy After Acute Carbon Monoxide Poisoning Accompanied with Flame Burn Injury

Case Report of Central Delayed Encephalopathy After Acute Carbon Monoxide Poisoning Accompanied with Flame Burn Injury

Effects of N-acetylcystein on changes in parvalbumin-positive interneurons in the hippocampus after carbon monoxide poisoning

Purpose: The purpose of this study was to investigate effect of N-acetylcysteine (NAC) on the injury of putative parvalbumin positive interneurons defined by molecular marker and hippocampal long-term potentiation (LTP), a marker of neural plasticity following acute carbon monoxide (CO) poisoning. Methods: Adult Sprague-Dawley rats were exposed to 1100 ppm CO for 40 minutes followed by 3000 ppm CO for 20 minutes. Animals received daily intraperitoneal injection of NAC (150 mg/kg) for 5 days after CO exposure. Changes in learning and spatial memory were evaluated by Y-maze test 5 days after the poisoning. In vivo LTP in hippocampal CA1 area was evaluated by using extracellular electrophysiological technique. Immunohistochemical staining were adopted to observe expressional damages of parvalbumin (PV) immunoreactive interneurons in the hippocampus following the poisoning. Results: Acute CO intoxication resulted in no changes in memory performance at Y-maze test but a significant reduction of LTP in the in hippocampal CA1 area. There was also a significant reduction of PV (+) interneurons in the hippocampal CA1 area 5 days after CO poisoning. Daily treatment of NAC significantly improved hippocampal LTP impairment and reduced immunoreactivity for PV in the hippocampus following the acute CO poisoning. Conclusion: The results of this study suggest that reduction of hippocampal LTP and PV (+) interneurons in the hippocampus is sensitive indicator for brain injury and daily NAC injections can be the alternative therapeutics for the injury induced by acute CO poisoning.

Potential markers for predicting delayed encephalopathy in patients with acute carbon monoxide poisoning

BackgroundAcute carbon monoxide poisoning (ACOP) commonly results in delayed neuropsychiatric sequelae (DNS). Currently, there are no reliable predictors. The aim of this article is to establish a practical model for predicting the development of delayed encephalopathy clinically. MethodsRetrospective analysis of clinical data were performed at a single institution for the past 6 years. 107 patients with ACOP were recruited, of who 67 developed DNS and 40 did not. Clinical characteristics of the patients were analyzed between the two groups. The risk factors associated with DNS development were screened to identify the potential markers for predicting DNS. A predictive model was then built, and the receiver operating characteristic (ROC) curve analysis was used to assess its predictive ability. ResultsThere were significant differences in 13 clinical features between the two groups. Four potential markers were identified. They were age, source of CO, Glasgow Coma Scale score and the initiation of HBOT. The potential predictive model showed an area under the curve (AUC) of 0.93 in the training set and 0.97 in the testing set. ConclusionsOur model could calculate the probability of DNS after acute CO poisoning.

Analysis of risk factors of delayed encephalopathy after acute carbon monoxide poisoning

Objective:To analyze the risk factors of delayed encephalopathy in patients with acute carbon monoxide poisoning (DEACMP) and to investigate the clinical significance and clinical value.Methods:The baseline data from 68 patients admitted in the 981st Hospital of Chinese People’s Liberation Army Joint Logistics Support Force were collected, including sex, age, Glasgow Coma Scale (GCS), history of smoking/drinking, history of DEACMP. Laboratory examination records including cranial CT/MRI, cervical vascular color ultrasonography, cardiac color ultrasonography, blood biochemical markers, blood routine, and blood coagulation function were also collected. Additionally, patients were followed-up visited at 1 month and 6 months. Patients were divided into either the DEACMP group or the NDEACMP group according to the occurrence of DEACMP. The risk factors of DEACMP were identified by univariate and logistic regression analyses. The area under the curve (AUC), sensitivity, and specificity of each index were compared by the receiver operating characteristic (ROC) curve.Results:Among the 68 patients, 13 patients suffered from DEACMP with an incidence of 19.1%. Univariate analysis indicated that there were statistically significant differences in patients’ age, blood glucose, blood glucose/potassium, GCS scores, abnormal cranial CT/MRI, and coma time more than 4 h (P &lt; 0.05). Logistic regression analysis showed that B, SE, Wald, df, P, Exp (B) of GCS score were -0.489, 0.208, 5.55, 1, 0.018 and 0.634, respectively. Overall, GCS score is correlated with DEACMP’s occurrence. ROC curve analysis showed that the sensitivity, specificity, and the AUC of GCS scores were 0.769, 0.873 and 0.843, respectively. The AUC of the indices in descending order are: GCS score, blood glucose, blood glucose/potassium and age.Conclusion:GCS score, blood glucose, blood glucose/potassium, and age are useful predictive factors for the occurrence of DEACMP. Among these, GCS score is the most significant predictive factor.

Frontal QRS-T angle as a predictive marker for myocardial damage in acute carbon monoxide poisoning.

The present study was undertaken to investigate the prognostic value of the frontal QRS-T angle associated with adverse cardiac outcomes in patients with carbon monoxide (CO) poisoning in early stages in the emergency department. The data of 212 patients with CO poisoning who were admitted to the ED between January 2010 and May 2020 were retrospectively analyzed. The frontal QRS-T angle was obtained from the automatic reports of the EKG device. Compared to patients without myocardial damage, among patients with myocardial damage, statistically high creatinine, creatine kinase MB, cardiac troponin I, and frontal QRS-T angle values were found (p < 0.001 for all parameters), while the saturation of arterial blood pH and arterial oxygen values were found to be lower (p = 0.002 and p < 0.001, respectively). The frontal QRS-T angle values were correlated with creatine kinase, creatine kinase-MB, cardiac troponin I, and oxygen saturation (SpO2) in arterial blood (r = 0. 232, p = 0.001; r = 0. 253, p = < 0.001; r = 0. 389, p = < 0.001; r = -0. 198, p = 0.004, respectively). The optimum cut-off value of the frontal QRS-T angle was found to be 44.5 (area under the curve: 0.901, 95% confidence interval: 0.814-0.988, sensitivity: 87%, specificity: 84%). The frontal QRS-T angle, a simple and inexpensive parameter that can be easily obtained from 12-lead surface electrocardiography, can be used as an early indicator in the detection of myocardial damage in patients with CO poisoning.

Therapeutic effect and molecular mechanism of Salvia Miltiorrhiza on rats with acute brain injury after carbon monoxide poisoning based on the strategy of internet pharmacology.

The pathogenesis of brain injury caused by carbon monoxide poisoning (COP) is very complex, and there is no exact and reliable treatment in clinic. In the present study, we screened the therapeutic target and related signal pathway of Salvia Miltiorrhiza for acute COP brain injury, and clarified the pharmacological mechanism of multicomponent, multitarget, and multisignal pathway in Salvia Miltiorrhiza by network pharmacology. To further verify the therapeutic effect of Salvia Miltiorrhiza on acute brain injury based on the results of network analysis, a total of 216 male healthy Sprague Dawley rats were collected in the present study and randomly assigned to a normal control group, a COP group and a Tanshinone IIA sulfonate treatment group (72 rats in each group). The rat model of acute severe COP was established by the secondary inhalation in a hyperbaric oxygen chamber. We found that Salvia Miltiorrhiza had multiple active components, and played a role in treating acute brain injury induced by COP through multiple targets and multiple pathways, among them, MAPK/ERK1/2 signaling pathway was one of the most important. COP can start apoptosis process, activate the MAPK/ERK1/2 signaling pathway, and promote the expression of VEGF-A protein and the formation of brain edema. Tanshinone IIA can effectively inhibit apoptosis, up-regulate the expressions of VEGF-A, P-MEK1/2 and P-ERK1/2 proteins, thereby protect endothelial cells, promote angiogenesis and microcirculation, and finally alleviate brain edema.

Abnormal Brain Functional Network Dynamics in Acute CO Poisoning.

Aims: Carbon monoxide poisoning is a common condition that can cause severe neurological sequelae. Previous studies have revealed that functional connectivity in carbon monoxide poisoning is abnormal under the assumption that it is resting during scanning and have focused on studying delayed encephalopathy in carbon monoxide poisoning. However, studies of functional connectivity dynamics in the acute phase of carbon monoxide poisoning may provide a more insightful perspective for understanding the neural mechanisms underlying carbon monoxide poisoning. To our knowledge, this is the first study that explores abnormal brain network dynamics in the acute phase of carbon monoxide poisoning.Methods: Combining the sliding window method and k-means algorithm, we identified four recurrent dynamic functional cognitive impairment states from resting-state functional magnetic resonance imaging data from 29 patients in the acute phase of carbon monoxide poisoning and 29 healthy controls. We calculated between-group differences in the temporal properties and intensity of dFC states, and we also performed subgroup analyses to separately explore the brain network dynamics characteristics of adult vs. child carbon monoxide poisoning groups. Finally, these differences were correlated with patients’ cognitive performance in the acute phase of carbon monoxide poisoning and coma duration.Results: We identified four morphological patterns of brain functional network connectivity. During the acute phase of carbon monoxide poisoning, patients spent more time in State 2, which is characterized by positive correlation between SMN and CEN, and negative correlation between DMN and SMN. In addition, the fractional window and mean dwell time of State 2 were positively correlated with coma duration. The subgroup analysis results demonstrated that the acute phase of childhood carbon monoxide poisoning had greater dFNC time variability than adult carbon monoxide poisoning.Conclusion: Our findings reveal that patients in the acute phase of carbon monoxide poisoning exhibit dynamic functional abnormalities. Furthermore, children have greater dFNC instability following carbon monoxide poisoning than adults. This advances our understanding of the pathophysiological mechanisms underlying acute carbon monoxide poisoning.