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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., (© 2024. The Author(s).)

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.

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 (HBO 2 ) 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 HBO 2 treatment were included in an HBO 2 group, while those who only received conventional drug treatment were included in a control group. HBO 2 was administered once daily. Patients in the HBO 2 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 HBO 2 group was greater than that in the control group (all P <0.05). The effective rate of the HBO 2 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 HBO 2 group was better than that in the control group., Conclusions: Hyperbaric oxygen can significantly relieve the symptoms of dementia in patients with DEACMP.

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., Competing Interests: The authors declare no conflict of interest., (© 2023 The Author(s). Published by IMR Press.)

Objective: To observe the effects of transcranial direct current stimulation (tDCS) on nerve injury markers and prognosis in patients with acute severe carbon monoxide poisoning (ASCOP) . Methods: In May 2021, 103 ASCOP patients were treated in the emergency department of Harrison International Peace Hospital of Hebei Medical University from November 2020 to January 2021. The patients were divided into two groups according to whether they received tDCS treatment. The control group (50 cases) were given oxygen therapy (hyperbaric oxygen and oxygen inhalation) , reducing cranial pressure, improving brain circulation and cell metabolism, removing oxygen free radicals and symptomatic support, and the observation group (53 cases) was treated with 2 weeks of tDCS intensive treatment on the basis of conventional treatment. All patients underwent at least 24 h bispectral index (BIS) monitoring, BIS value was recorded at the hour and the 24 h mean value was calculated. Neuron-specific enolase (NSE) and serum S100B calcium-binding protein (S100B) were detected after admission, 3 d, 7 d and discharge. Follow-up for 60 days, the incidence and time of onset of delayed encephalopathy (DEACMP) with acute carbon monoxide poisoning in the two groups were recorded. Results: The NSE and S100B proteins of ASCOP patients were significantly increased at admission, but there was no significant difference between the two groups ( P =0.711, 0.326) . The NSE and S100B proteins were further increased at 3 and 7 days after admission. The increase in the observation group was slower than that in the control group, and the difference was statistically significant ( P (3 d)=0.045, 0.032, P (7 d)=0.021, 0.000) ; After 14 days, it gradually decreased, but the observation group decreased rapidly compared with the control group, with a statistically significant difference ( P =0.009, 0.025) . The 60 day follow-up results showed that the incidence of DEACMP in the observation group was 18.87% (10/53) , compared with 38.00% (19/50) in the control group ( P =0.048) ; The time of DEACMP in the observation group[ (16.79±5.28) d] was later than that in the control group[ (22.30±5.42) d], and the difference was statistically significant ( P =0.013) . Conclusion: The early administration of tDCS in ASCOP patients can prevent the production of NSE and S100B proteins, which are markers of nerve damage. and can improve the incidence and time of DEACMP.

Introduction: Carbon monoxide (CO) poisoning can cause serious neurological sequelae. However, there is neither effective treatment strategy nor reliable indicators to determine the prognosis of patients with CO poisoning. The present study aimed to observe the changes of neurological function score, disease severity score, cerebral oxygen utilization (O 2 UCc), bispectral (BIS) index and neuron-specific enolase (NSE) concentration, and to elucidate the clinical significance of these potential indicators and the neuroprotective effect of mild hypothermia on brain injury in patients with severe acute CO poisoning., Materials and Methods: A total of 277 patients with acute severe CO poisoning from 2013 to 2018 were enrolled in our hospital. Patients were divided into three groups according to their body temperature on the day of admission and their willingness to treat: a fever group (n = 78), a normal temperature group (NT group, n = 113), and a mild hypothermia group (MH group, n = 86). All patients were given hyperbaric oxygen therapy, while those in the MH group received additional mild hypothermia treatment. The severity of the disease, the neurobehavioral status, the incidence of delayed encephalopathy after acute carbon monoxide poisoning (DEACMP), and other indicators including BIS, O 2 UCc, NSE were further evaluated in all patients at given time-points., Results: Mild hypothermia therapy improved the prognosis of patients with CO poisoning, significantly decreased the value of O 2 UCc and NSE, and up-regulated BIS. The incidence of DEACMP at 6 months was 27% in the fever group, 23% in the NT group, and 8% in the MH group. The values of Glasgow-Pittsburgh coma scale (G-P score), BIS index and NSE were closely related to the occurrence of DEACMP, the cutoff values were 12.41, 52.17 and 35.20 ng/mL, and the sensitivity and specificity were 79.3%, 77.6%, 79.3% and 67.6%, 89.5%, 88.6% in the receiver operating characteristic curve (ROC), respectively., Conclusions: Early mild hypothermia treatment could significantly reduce the severity of brain injury after CO poisoning, and might be further popularized in clinic. G-P scores, NSE and BIS index can be regarded as the prediction indicators in the occurrence and development of DEACMP., Clinical Trial Registration: The study protocol was granted from Qingdao University Research Ethics Committee (Clinical trial registry and ethical approval number: QD81571283)., Competing Interests: Declaration of Competing Interest None., (Copyright © 2022 Elsevier Inc. All rights reserved.)

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.

Background Delayed encephalopathy (DE) is the most severe complication after acute carbon monoxide (CO) poisoning, which seriously affects the outcome of patients and leads to a high disability rate. Prior studies have shown that hyperbaric oxygen (HBO 2 ) therapy is therapeutic for DE due to reducing immune-mediated neuropathology and thus improving cognitive performance. Methods In our present perspective study, five DE patients were treated regularly with HBO 2 therapy. The mini-mental state examination (MMSE) and Barthel index (BI) were intermittently collected during their hospitalization for mental and physical status evaluation, the peripheral bloods were serially sampled to determine the concentration changes of circulating stem cells, as well as corresponding BDNF and neural markers. Results MMSE and BI showed series of improvements after multiple HBO 2 therapies. The CD34 + /CD90 + and CD34 + /CD133 + dual positive cells, which were categorized as circulating stem cells, were observed an overall up-regulation since the beginning of the DE onset upon the application of HBO 2 therapy. Characteristic neurotrophin BDNF, neural markers such as nestin and synaptophysin (SYP) were also up-regulated after exposure of HBO 2 . Conclusion The application of HBO 2 therapy is of significance in improving the cognition of DE patients, along with mobilized circulating stem cells. We primarily infer that the CD34 + /CD90 + and CD34 + /CD133 + cells were mobilized by HBO 2 exposure and have played a positive role in cognition improvement on DE patients by up-regulation of BDNF, nestin and SYP. The altering amount of circulating stem cells mobilized in peripheral blood could be a potential marker on predicting the outcome of DE., Competing Interests: Declaration of competing interest We have no competing interests to declare., (Copyright © 2021 Elsevier Inc. All rights reserved.)

Objective: To study the clinical manifestations, magnetic resonance imaging (MRI) findings, and prognosis of delayed encephalopathy after carbon monoxide poisoning (DEACMP)., Methods: The medical records of 20 patients with DEACMP were retrospectively reviewed. All the patients received hyperbaric oxygen treatment and other treatments as necessary., Results: The patients had diverse clinical manifestations, including memory deficits, personality changes, cognitive or executive function deficits, mood disorders, Parkinsonism, dystonia or other motor impairments, and akinetic mutism. MRI revealed lesions in the bilateral cerebral white matter and/or basal ganglia. Except for the pathologically confirmed DEACMP, epileptic seizure, hemiplegia, and vegetative state, the remaining symptoms had been improved, especially the cognitive impairment, which had been decreased from 95% to 25% and psychiatric symptoms also decreased from 95% to 55% at the 6-month follow-up., Conclusions: The prognosis of patients with DEACMP was poor, and they had a relatively severe disability. The early use of hyperbaric oxygen is of great significance to improve clinical efficacy and get a better prognosis., Competing Interests: The authors declare that there is no conflict of interest regarding the publication of this article., (Copyright © 2020 Jinzhi Liu et al.)

Objective: To investigate the effect of transcranial direct current stimulation (tDCS) on cognitive function of delayed encephalopathy after carbon monoxide poisoning (DEACMP) . Methods: A total of 58 patients with DEACMP admitted to the Emergency Medicine Department of Hudson International Peace Hospital from January 2018 to January 2020 were included. According to the random number table, the patients were randomly divided into study group and control group, with 29 patients in each group. Patients in both groups were given nutritional nerve therapy, improved microcirculation, adrenal cortical hormone and other drugs, as well as hyperbaric oxygen and rehabilitation training, once per day. The study group was treated with tDCS (electrode pads were placed and current stimulation was given 30 min/time) 1/d on the basis of conventional treatment, while the control group was treated with tDCS pseudo stimulation (electrode pads were placed and current stimulation was given for 10 s) 1/d for 30 days consecutively. The auditory event-related potential P300 (ERP-P300) was tested before and 30 days after treatment, and the Mini-Mental State Examination (MMSE) scale, Barthel index (BI) and the National Institutes of Health Neurological Impairment score (NIHSS) were used to evaluate and analyze the patients. Results: There was no significant difference in scores between the two groups before treatment (all P >0.05) . After 30 days of treatment, the MMSE score, orientation, memory, attention and computing power, and language ability of the study group were all higher than those of the control group, and the differences were statistically significant ( P <0.05) . 90 days after treatment, the BI of the study group was higher than that of the control group ( P <0.05) . After 30 days of treatment, the NIHSS score of the study group was significantly lower than that of the control group ( P <0.05) . The latency of ERP-P300 in the study group was shorter than that in the control group, and the amplitude was higher than that in the control group at 30 days after treatment, and the difference was statistically significant ( P <0.05) . The latency of ERP-P300 was negatively correlated with the total MMSE score before and after DEACMP treatment ( r =-0.837, -0.819, P <0.05) . The latency of ERP-P300 was negatively correlated with orientation, attention and computing power, and language ability before treatment ( r =-0.698, -0.675, -0.742, P <0.05) . Conclusion: TDCS treatment can help improve the cognitive function of DEACMP patients, and ERP-P300 test can help determine the cognitive function severity of patients.

Objective: To study the expression of high mobility group protein 1 (HMGB1) in the brain of rats after hyperbaric oxygen (HBO) treatment of acute carbon monoxide poisoning (DEACMP) , and to explore the mechanism of HBO in the prevention and treatment of DEACMP pathological process by regulating HMGB1. Methods: 108 SD rats were randomly divided into control group (NC group) and co group (CO group) . HBO treatment group (HBO group) , 48 rats in each group. Co group and HBO group were used to establish CO poisoning model, HBO group were treated with hyperbaric oxygen once a day. Water maze test was used to detect and analyze the memory retention ability of three groups of rats in 3 d, 7 d, 14 d. ELISA was used to detect the plasma concentration of HMGB1、IL-6、TNF-α in three groups of rats on the 1 d, 3 d, 7 d, 14 d, 21 d Concentration. Western blotting was used to detect the expression of HMGB1 and Caspase-3 in the brain of the three groups on the 1 d, 3 d, 7 d, 14 d, 21 d. TUNEL staining was used to detect the apoptosis of hippocampal neurons in the three groups. Results: Compared with NC group, the average escape latency of rats in CO group and HBO group was significantly prolonged, and the activity time of platform quadrant in CO group was significantly shortened on 14 d and 21 d ( P <0.05) ; compared with CO group, the average escape latency of HBO group on 7 d, 14 d and 21 d was significantly shortened ( P <0.05) . Compared with NC group, plasma HMGB1 in CO group and HBO group were significantly increased ( P <0.05) ; after 3 days, HBO group was significantly lower than co group, the difference was statistically significant ( P <0.05) . The levels of IL-6 and TNF-α in HBO group and co group increased rapidly and then decreased gradually. The increased levels of IL-6 and TNF-α in HBO group were significantly lower than those in CO group ( P <0.05) . Compared with NC group, the expression of HMGB1 and Caspase-3 in CO group was significantly increased on 3 d, 7 d and 14 d ( P <0.05) ; the expression of HMGB1 and Caspase-3 in HBO group was significantly increased on 3 d, 7 d, 14 d and 21 d ( P <0.05) ; compared with CO group, the expression of HMGB1 and Caspase-3 in HBO group decreased significantly on 3 d, 7 d, 14 d and 21 d ( P <0.05) . The apoptotic index of nerve cells in CO group began to increase at 3 days, which was significantly different from that of NC group ( P <0.05) , and the difference was still statistically significant on 21 d ( P <0.05) ; the apoptotic index of nerve cells in HBO group was slightly increased, but there was no significant difference compared with NC group ( P >0.05) , and the apoptotic index of 3 d, 7 d, 14 d and 21 d in HBO group was significantly lower than that in CO group ( P <0.05) . Conclusion: acute CO poisoning can induce the release of HMGB1 and a variety of inflammatory factors. HMGB1 can promote the apoptosis of nerve cells after acute CO poisoning by up regulating the expression of caspase-3 protein, and participate in the pathological process of DEACMP. HBO can down regulate the expression of HMGB1, IL-6, TNF-α and caspase-3 protein, inhibit the apoptosis of nerve cells, and play a protective role on nerve cells.

Background: 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., Patients and Methods: 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., Results: 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., Conclusion: 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., Competing Interests: The authors report no conflicts of interest in this work., (© 2020 Zhang et al.)

Diffusion tensor imaging of the brain tissue microstructure was performed to predict or diagnose the pathophysiological mechanism underlying delayed encephalopathy after carbon monoxide poisoning and the treatment effect was analyzed. The changes in the diffusion parameters (average diffusion coefficient and fractional anisotropy) in adult patients after hyperbaric oxygen therapy of delayed encephalopathy after carbon monoxide poisoning were not significant differences of the two lateral ventricles or anterior or posterior limb of the internal capsule. In the group exposed to hyperbaric oxygen therapy, the fractional anisotropy values of the white matter in the ventricles of the brain and anterior and posterior limbs of the internal capsule were higher than those recorded before therapy, while the average diffusion coefficient values were significantly lower. These finding provide important monitoring indicators for clinicians., Competing Interests: All authors declare no conflict of interest., (© 2019 Wu et al. Published by IMR press.)

Objective: To study the clinical effect of high pressure oxygen and Butylphthalide in the recovery of cerebral metabolism after carbon monoxide poisoning. Methods: 84 patients treated from May 2014 to May 2016 in our hospital were selected. The subjects were randomly and equally divided into two groups. The control group adopted the conventional therapy and high pressure oxygen; on the basis, the observation group also took Butylphthalide. The clinical effect, duration of coma, recovery of consciousness, incidence rate of delayed encephalopathy was observed. After 1m of treatment, the HDS point was evaluated. Results: The total effective rate of control group (76.19%, 32/42) was lower than that of observation group (95.24%, 40/42) ( P <0.05) . The duration of coma for observation group was shorter than that of control group. The percentage for patients with recovery of consciousness and incidence rate of delayed encephalopathy for observation group was better than that of control group ( P <0.05) . The HDS point for observation group was even higher than that of control group ( P <0.05) . Conclusion: The high pressure oxygen and butylphthalide can improve the clinical effective rate, shorten the duration of coma and promote the patient's recovery of consciousness. It is worthy of clinical promotion.

Objective: To investigate the dynamic change in cerebral oxygen utilization coefficient (O(2)UCc) in the early stage of acute severe carbon monoxide poisoning (ASCMP) and its value in predicting delayed encephalopathy after acute carbon monoxide poisoning (DEACMP) . Methods: A prospective observational study was conducted for patients with ASCMP who were admitted to our hospital from November 2013 to March 2016, and their baseline features and physiological parameters were recorded. Observation ended at two months after acute poisoning; according to the presence or absence of DEACMP, the patients were divided into DEACMP group with 21 patients and non-DEACMP group with 64 patients. The change in O(2)UCc was monitored on admission and at 6, 24, 48, and 72 hours. Spearman correlation was used to investigate the correlation between O(2)UCc and Acute Physiology and Chronic Health Evaluation II (APACHE II) score, and the receiver operating characteristic (ROC) curve was used to evaluate the accuracy of O(2)UCc in predicting DEACMP. Results: Both groups had a significant increase in O(2)UCc on admission, and the DEACMP group had a significantly greater increase than the non-DEACMP group (52.57%±9.30% vs 41.46±%6.37%, P <0.05) . Then both groups tended to have a reduction in O(2)UCc, and the DEACMP group had a significantly higher O(2)UCc than the non-DEACMP group at 6, 24, and 48 hours (47.40%±7.92%, 39.38%±8.01%, and 32.29%±6.31% vs 34.51%±7.89%, 28.79%±5.4%, and 27.72%±5.46%, P <0.05) . On admission and at 6, 24, and 48 hours, O2UCc was positively correlated with APACHE II score ( r =0.304, 0.398, 0.426, and 0.300, P =0.005, 0.000, 0.000, and 0.005) . The ROC curve showed that O(2)UCc had a value in predicting DEACMP on admission and at 6, 24, and 48 hours, and 6-hour O2UCc had the highest predictive value with an area under the ROC curve of 0.870 (95% confidence interval 0.794-0.947, P <0.05) . Conclusion: The dynamic change in O(2)UCc has a reference value in early identification of DEACMP, and O(2)UCc can be used as an important reference index for predicting DEACMP.

BACKGROUND Delayed encephalopathy after acute carbon monoxide (CO) poisoning (DEACMP) is one of the most serious complications after CO poisoning. This study was conducted to explore the efficacy of the combined application of N-Butylphthalide and hyperbaric oxygenation therapy (HBO) on cognitive dysfunction in patients with DEACMP. MATERIAL AND METHODS A total of 184 patients with DEACMP were randomly assigned to either receive HBO or N-Butylphthalide and HBO. Meanwhile, all patients received conventional treatment. The total remission rate (RR) was used to assess the clinical efficacy. The Mini-Mental State Examination (MMSE) was used to assess the cognitive function, and the National Institutes of Health Stroke Scale (NIHSS) was used to assess the neurological function. RESULTS Finally, there were 90 and 94 patients in the control and experimental groups, respectively. After eight weeks of treatment, the total RR in the experimental group (47.9%) was significantly higher than that in the control group (33.3%). Compared to the control group, significantly more patients in the experimental group had MMSE scores of 24-30. The lower NIHSS score in the experimental group showed that N-Butylphthalide had the effect of preservation and restoration of neurological function. No obvious drug toxicity or liver and kidney dysfunction was observed, and there was no significant change in the level of blood glucose and blood lipids. CONCLUSIONS These results indicated that the combined application of N-Butylphthalide and HBO could significantly improve the cognitive dysfunction of patients with DEACMP and have great clinical efficacy, which should be further studied.

Background: Delayed encephalopathy after acute carbon monoxide (CO) poisoning (DEACMP) commonly occurs after recovering from acute CO poisoning. This study was performed to assess the efficacy of the combined application of dexamethasone and hyperbaric oxygen (HBO) therapy in patients with DEACMP., Patients and Methods: A total of 120 patients with DEACMP were recruited and randomly assigned into the experimental group (receiving dexamethasone 5 mg/day or 10 mg/day plus HBO therapy) and control group (HBO therapy as monotherapy). Meanwhile, the conventional treatments were provided for all the patients. We used the Mini-Mental State Examination (MMSE) scale to assess the cognitive function, the National Institutes of Health Stroke Scale (NIHSS) to assess the neurological function and the remission rate (RR) to assess the clinical efficacy. Myelin basic protein (MBP) in the cerebrospinal fluid (CSF) was also measured., Results: After 4 weeks of treatment, compared to the control group, the experimental group had a significantly higher remission rate ( P =0.032), a significantly higher average MMSE score ( P =0.037) and a significantly lower average NIHSS score ( P =0.002). Meanwhile, there was a trend toward better improvement with dexamethasone 10 mg/day, and the level of MBP in the CSF of patients was significantly lower in the experimental group than in the control group ( P <0.0001). The addition of dexamethasone did not significantly increase the incidence of adverse events., Conclusion: These results indicate that the combined application of dexamethasone and HBO therapy could yield better efficacy for patients with DEACMP and should be viewed as a potential new therapy., Competing Interests: Disclosure The authors report no conflicts of interest in this work.

Delayed encephalopathy after carbon monoxide (CO) poisoning (DEACMP) is still a clinical challenge. This study aimed to investigate the efficacy of combined therapy of mesenchymal stem cell (MSC) transplantation and butylphthalide in DEACMP patients.Forty-two DEACMP patients were treated with 1 of the 3 therapies: combined therapy of MSC transplantation and butylphthalide; MSC transplantation alone; or hyperbaric oxygen therapy. The MSCs were alternatively injected into the subarachnoid space and the carotid artery using a self-made high-pressure injector. The Mini-Mental State Examination and the Barthel index of activities of daily living were administered before the treatment, and at 1 month, 3 months, and 6 months after the treatment. Computed tomography and magnetic resonance imaging results before and after the treatment were compared.At 1 month, 3 months, and 6 months after the treatment, the Mini-Mental State Examination scores and the Barthl scores were significantly higher in patients with the combined therapy of MSC transplantation and butylphthalide than those in patients with MSC transplantation alone or hyperbaric oxygen therapy (all P < 0.0001). No significant adverse events occurred.The combination of MSC transplantation and butylphthalide is safe and effective in treating DEACMP., Competing Interests: The authors report no conflicts of interest.

Carbon monoxide poisoning is the most common cause of fatal poisoning worldwide and can lead to severe brain damages. We report a delayed encephalopathy after a severe carbon monoxide poisoning with uncommon magnetic resonance imaging findings.

In CO-poisoned patients without loss of consciousness no significant long-term functional differences in outcome have been shown in any hyperbaric versus normobaric oxygen studies. Since brain histology changes cannot be studied in CO-poisoned patients we evaluated the efficacy of normobaric and hyperbaric oxygen therapy in preventing brain cell injury in CO-poisoned animals without loss of consciousness. Wistar rats without loss of consciousness after exposure to 3000ppm of CO for 60min were exposed to ambient air (group 1), 100% oxygen at a pressure of 1bar (group 2) and 100% oxygen at a pressure of 3bar (group 3). The rats were sacrificed after two weeks, brain samples were stained with hematoxylin-eosin and a percentage of pyknotic cells in hippocampus was reported. Analyses of differences in percentage of pyknotic cells between different kinds of therapy showed that the percentage of pyknotic cells of the second group (2.3+/-1.2%) treated with normobaric oxygen and the third group (4.5+/-4.0%) treated with hyperbaric oxygen were similar, and both of them were significantly different, with a much lower percentage of pyknotic cells, from the first group left on ambient air (47.7+/-10.0%). In conclusion, immediate normobaric and hyperbaric oxygen therapy equally prevents hippocampal cell injury in CO-poisoned rats without loss of consciousness.

The role of brain computerized tomography (CT) imaging in predicting clinical outcome was investigated in patients receiving hyperbaric oxygen therapy for serious carbon monoxide (CO) poisoning. From a series of 48 consecutive patients suffering loss of consciousness from CO exposures, the records of 40 selected patients were evaluated to determine how their CT findings correlated with clinical outcome. A neuroradiologist blinded to patient outcome confirmed the radiographic findings. CT abnormalities consisted of globus pallidus hypodensities (nine patients), subcortical white matter hypodensities (four), cerebral cortical lesions (one), cerebral edema (one), hippocampal lesions (one), and complete loss of gray-white differentiation (one). Of the patients with globus pallidus lesions, 44% manifested incomplete recovery, whereas white matter lesions reflected a 74% incidence of morbidity. Age, duration of CO exposure, and interval between CO exposure and treatment did not significantly relate to clinical outcome. The blood carboxyhemoglobin levels correlated with clinical prognosis (P < 0.05) and, importantly, CT results significantly predicted clinical outcome (P < 0.05). A normal scan correlated highly with a complete recovery, whereas an abnormal scan predicted incomplete recovery or death, despite prior HBO therapy. The current study establishes prognostic validity for brain CT imaging for evaluating clinical outcome after HBO therapy for CO poisoning.

Study Objective: To investigate whether topographic analysis of EEG mapping and technetium-99m (99mTc) hexamethylpropylenamine oxide (HMPAO) brain single-photon emission computed tomography (SPECT) can detect cerebral anomalies in the acute phase of carbon monoxide poisoning., Design: Twelve patients aged 18 to 55 years with severe carbon monoxide poisoning and no history of neurologic disorder were evaluated. Either nasal (5 patients) or hyperbaric (7 patients) oxygen therapy was administered. Criteria for hyperbaric oxygen therapy were blood CO of more than 20%, loss of consciousness, pregnancy, or signs of cardiac injury. After oxygen treatment, all patients had a blood CO value of 0% and no patient had persistent acute signs of toxicity. Patients then were investigated by confentional EEG, EEG mapping, and 99mTc HMPAO brain SPECT. These procedures were performed on the day of admission., Participants: After nasal (5 patients) or hyperbaric (7 patients) oxygen therapy was administered, 12 adults with severe carbon monoxide poisoning were evaluated. All studies were performed on the day of admission., Measurements: Conventional EEG, EEG mapping, and 99mTc HMPAO brain SPECT., Results: While classic EEG was normal in 9 of 12 patients and showed diffuse anomalies in 3, EEG mapping and 99mTc HMPAO brain SPECT demonstrated unilateral or bilateral regional anomalies in 8 of 12 patients. Anomalies were localized in temporo-parieto-occipital areas, the watershed areas of the major cerebral arteries, or in temporal cortex., Conclusion: These preliminary results suggest that EEG mapping and 99mTc HMPAO brain SPECT can be complementary tools to diagnose early regional cerebral anomalies in carbon monoxide-poisoned patients.

Recent animal and clinical data require a reevaluation of the traditional approach to the patient exposed to carbon monoxide. Unfortunately, these new data are inconclusive and generate controversies regarding the indications and value of neuropsychologic testing, cause of carbon monoxide toxicity, and indications (if any) for hyperbaric oxygen therapy. These controversies and their implications for the emergency physician are discussed.

Two cases are presented to illustrate the delayed neurological complications which may follow carbon monoxide (CO) poisoning, the mechanisms of which are not well known and which do not seem to be recognized widely enough to safeguard patients. Broad discussion is needed to determine how cases of CO exposure/poisoning should best be handled if sequelae are to be avoided.