Acute Severe Carbon Monoxide Poisoning Research Articles

Prognostic value of systemic immune-inflammation index and monocyte-to-HDL-cholesterol ratio in early cardio-cerebral complications in elderly patients with acute severe carbon monoxide poisoning

To investigate how effectively systemic immune-inflammation index (SII) and Monocyte-to-HDL-cholesterol ratio (MHR) predict the development of early cardio-cerebral complications in elderly patients who have experienced acute severe carbon monoxide poisoning (ASCMP). A retrospective analysis was conducted on 77 elderly patients with ASCMP admitted to the emergency department of Harrison International Peace Hospital from November 2020 to March 2022. The prevalence of early-onset complications among the 77 individuals was 38.96%. Binary Logistics regression analysis showed that SII and MHR were independent influencing factors of early cardio-cerebral complications in elderly patients with ASCMP. The complication group had a longer length of stay, a greater mortality rate, and a higher incidence of delayed encephalopathy after acute carbon monoxide poisoning (p < .05) than the non-complication group. The area under the curve (AUC) of SII and MHR in predicting early cardio-cerebral complications in elderly patients with ASCMP were 0.724 and 0.796, respectively, with 80.0% and 63.3% sensitivity, and 61.7% and 87.2% specificity. The incidence of early cardio-cerebral complications in elderly patients who had ASCMP is high and the prognosis is poor. SII and MHR can be utilized as independent predictors of early cardio-cerebral complications in elderly patients with ASCMP, allowing doctors to diagnose and treat cardio-cerebral complications earlier and improve prognosis.

Effect of transcranial direct current stimulation on neurological injury markers and prognosis in patients with acute and severe carbon monoxide poisoning

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.

Clinical application of BIS combined with LCR in assessing brain function and prognosis of patients with severe carbon monoxide poisoning

BackgroundThis study investigated the value of the bispectral index (BIS) and lactate clearance rate (LCR) in the assessment of cerebral neurological injury and prognosis in acute severe carbon monoxide poisoning (ASCOP) patients. MethodsA retrospective study was conducted on 86 ASCOP patients admitted to our hospital from November 2019 to March 2021. The patients' prognosis neurological function of the brain after 3 months of treatment was observed. The patients were divided into good (48) and poor (38) groups according to the different prognoses. The GCS-Pittsburgh score (G-P score) was performed on the patients after admission. BIS and LCR were recorded at admission, 6 h, 24 h, 48 h, and 72 h after admission. We conducted correlation and multivariate regression analysis for each factor. ROC curves were used to assess the diagnostic efficacy of each index on prognosis. ResultsThe two different prognosis groups showed that there were no significant differences for gender, age, treatment-free period, and APACHE II score at admission (P > 0.05); the G-P score, the BIS, and LCR at different times of admission was significantly higher in the good group than in the poor group (all P < 0.05). Both the 24 h of BIS and the LCR were diagnostically superior to the G-P score (P < 0.05); the diagnostic efficacy of the two combined was not superior to that of the individual factors (AUC=0.787), but had a high specificity (93.8 %). ConclusionBIS monitoring and LCR have clinical value in the assessment of neurological damage and prognostic in ASCOP patients.

Clinical significance of bispectral index monitoring in patients with acute severe carbon monoxide poisoning

Objective: To analyze the correlation of bispectral index (BIS) with the prognosis of patients with acute severe carbon monoxide poisoning (ASCMP) and its predictive value of adverse outcomes. Methods: In March 2021, 106 ASCMP patients who were treated in Harrison International Peace Hospital Affiliated to Hebei Medical University from January 2019 to December 2020 were taken as research objects. All patients underwent 24-hour BIS monitoring after admission, and were divided into good prognosis group (n=75) and poor prognosis group (n=31) according to the prognosis of the patients' cranial nerve function after 60 d. The general conditions, Acute Physiology and Chronic Health Evaluation Ⅱ (APACHEⅡ) score, Glasgow Coma Scale (GCS) score at admission and 24-hour BIS mean were compared between the two groups. Pearson correlation analysis was used to analyze the correlations between the 24-hour BIS mean and GCS score at admission, APACHEⅡ score and coma time. The receiver operating characteristic (ROC) curve was drawn to analyze the predictive value of 24-hour BIS mean, GCS score at admission, APACHEⅡ score and coma time on adverse outcome of ASCMP patients. Results: The coma time and APACHEⅡ score of the patients in the poor prognosis group were significantly higher than those in the good prognosis group, the GCS score at admission and 24-hour BIS mean were significantly lower than those in the good prognosis group (P<0.05) . Pearson correlation analysis showed that the 24-hour BIS mean was positively correlated with the GCS score at admission, and negatively correlated with the APACHEⅡ score, coma time (r=0.675, -0.700, -0.565, P<0.001) . The 24-hour BIS mean had the highest predictive value for adverse outcome of ASCMP patients, with a cut-off value of 74, the area under the curve was 0.883 (95%CI: 0.814-0.951, P<0.001) , and the sensitivity and specificity were 73.3% and 87.1%, respectively. Conclusion: The 24-hour BIS mean has a good correlation with the acute brain nerve injury, the severity of the disease and coma time of patients with ASCMP. And it has a high predictive value for the adverse outcome in patients with ASCMP.

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.

Neuroprotective effect of targeted regulatory Nrf2 gene on rats with acute brain injury induced by carbon monoxide poisoning.

Oxidative stress has been considered as an important cause of neurocyte damage induced by carbon monoxide (CO) poisoning; however, the precise mechanisms are not fully understood. The study aimed to elucidate the molecular mechanism and the neuroprotective effect of targeted regulatory nuclear factor erythroid2-related factor 2 (Nrf2) gene on acute brain injury in CO poisoning rats. An acute CO poisoning rat model was established by CO inhalation in hyperbaric oxygen chamber and followed by the administration of Nrf2 gene-loaded lentivirus. Mitochondrial membrane potential (ΔΨM), the levels of Nrf2, glutamate-cysteine ligase catalytic subunit (GCLC), catalase (CAT) and glutathione peroxidase (GSH-Px), and cell apoptosis were determined in brain tissue in rats. We found that CO poisoning could decrease ΔΨm of cells, slightly increase the expressions of Nrf2 and GCLC at mRNA and protein levels, reduce CAT and GSH-Px, and thus initiate apoptosis process. The Nrf2 gene treatment could obviously enhance the expressions of Nrf2 at mRNA and protein levels, and increase the concentrations of CAT and GSH-Px, maintain the ΔΨm of cells in brain tissue, significantly inhibit cell apoptosis as compared with the CO poisoning group (p < .05). These findings suggest that CO poisoning could induce oxidative stress and impair mitochondrial function of cells in brain tissue. The administration of Nrf2 gene could notably strengthen the antioxidant capacity of cells through regulating the downstream genes of Nrf2/antioxidant responsive element signal pathway, and positively protect cells against brain injury induced by acute severe CO poisoning.

Correlation between early eeg dual-frequency index monitoring combined with lactic acid clearance rate and delayed encephalopathy with acute severe carbon monoxide poisoning

Objective: To analyze the correlation and predictive value between early BIS monitoring combined with lactic acid resolution (LCR) and delayed encephalopathy with acute severe carbon monoxide poisoning (ASCMP) . Methods: Select 96 cases of our hospital ASCMP patients were analyzed retrospectively in March 2020, and follow-up of 60 days, according to the outcome in patients with acute carbon monoxide poisoning (DEACMP) delayed encephalopathy group with good prognosis, compare two groups of general information, admission BIS average 24 h and 24 h after treatment the LCR, According to the 24h LCR test results, patients were divided into high LCR group (LCR>15%) and low LCR group (LCR≤15%) , analysis the BIS average, the correlation of the LCR with DEACMP and both individual and joint of DEACMP predictive value, Comparing clinical data of patients with high LCR and low LCR. Results: The mean BIS value of the DEACMP group 24 hours after admission was significantly lower than that of the group with good prognosis (P< 0.05) . LCR of DEACMP group was significantly lower than that of the group with good prognosis after 24 h treatment (P<0.05) . The prevalence of DEACMP in patients with high LCR was significantly lower than that with low LCR (P<0.01) ; In the early stage, BIS mean, LCR and DEACMP were negatively correlated (P< 0.05) , and the area under the curve predicted by BIS mean, LCR and their combination on DEACMP was 0.799, 0.847 and 0.902, respectively. Conclusion: Early BIS monitoring combined with LCR has a significant correlation with DEACMP, and the combined effect of the two is better. Early BIS combined with LCR detection can provide effective guidance for the prognosis assessment of ASCMP patients.

Effects of Early Ulinastatin Injection Combined With Hyperbaric Oxygen on Myocardial Enzymes and Cognitive Function in Patients with Acute Moderate and Severe Carbon Monoxide Poisoning

To observe the effect of early ulinastatin injection combined with hyperbaric oxygen on myocardial enzyme and cognitive function in patients with acute moderate and severe carbon monoxide poisoning. From May 2017~December 2020, 104 patients with acute carbon monoxide poisoning coma were divided into groups according to their treatment plan, 52 cases in the control group were treated with hyperbaric oxygen. Ulastatin group 52 cases were treated with early ulastatin injection combined with hyperbaric oxygen. The curative effect and incidence of delayed encephalopathy were counted, the average recovery time of the two groups was recorded, the changes of Hasegawa dementia scale score and Mini mental state examination score were compared between the two groups and the differences of blood gas index, myocardial enzyme index, and oxidative stress index and blood viscosity were detected. Ulinastatin group had higher efficacy than the control group (p<0.05). The blood oxygen partial pressure and superoxide dismutase increased in ulinastatin group and control group. The blood carbon dioxide partial pressure, creatine kinase, creatine kinase isoenzyme, aspartate aminotransferase, lactate dehydrogenase and malondialdehyde, catalase, lipid peroxide decreased. The oxygen partial pressure, superoxide dismutase of ulinastatin group after treatment was higher than that of control group, carbon dioxide partial pressure, myocardial enzyme index and malondialdehyde, catalase, lipid peroxide were lower than those of control group (p<0.05). The whole blood (high and low cut) viscosity and plasma viscosity of ulinastatin group and control group decreased, the Hasegawa dementia scale score and Mini mental state examination score increased and the blood viscosity of ulinastatin group was lower than that of control group after treatment and the Hasegawa dementia scale score and Mini mental state examination score were higher than that of control group (p<0.05).Average recovery time of ulinastatin group was shorter than that of control group and the incidence of delayed encephalopathy was lower than that of control group (p<0.05). Early ulinastatin injection combined with hyperbaric oxygen in the treatment of acute carbon monoxide poisoning coma can reduce oxidative stress injury, reduce myocardial enzyme expression and blood viscosity, improve blood gas index, promote patients to wake up and reduce the occurrence of delayed encephalopathy. It is worthy of clinical recommendation.

Effects of Adjunctive Therapeutic Hypothermia Combined With Hyperbaric Oxygen Therapy in Acute Severe Carbon Monoxide Poisoning.

To determine the effects of adjunctive therapeutic hypothermia, by comparing hyperbaric oxygen therapy versus hyperbaric oxygen therapy combined with therapeutic hypothermia in acute severe carbon monoxide poisoning. Retrospective analysis of data from our prospectively collected carbon monoxide poisoning registry. A single academic medical center in Wonju, Republic of Korea. Patients with acute severe carbon monoxide poisoning older than 18 years. Acute severe carbon monoxide poisoning was defined as mental status showing response to painful stimulus or unresponsive at the emergency department, and a continuation of this depressed mental status even after the first hyperbaric oxygen therapy. Patients were classified into the no-therapeutic hypothermia and therapeutic hypothermia groups. Hyperbaric oxygen therapy was performed up to twice within 24 hours after emergency department arrival, whereas therapeutic hypothermia was performed at a body temperature goal of 33°C for 24 hours using an endovascular cooling device after the first hyperbaric oxygen therapy. Hyperbaric oxygen therapy versus hyperbaric oxygen therapy combined with therapeutic hypothermia. We investigated the difference in the Global Deterioration Scale score at 1 and 6 months after carbon monoxide exposure, between the no-therapeutic hypothermia and therapeutic hypothermia groups. Global Deterioration Scale scores were classified as follows: 1-3 points (favorable neurocognitive outcome) and 4-7 points (poor neurocognitive outcome). During the study period, 37 patients were treated for acute severe carbon monoxide poisoning, with 16 and 21 patients in the no-therapeutic hypothermia and therapeutic hypothermia groups, respectively. The therapeutic hypothermia group demonstrated significantly higher number of patients with favorable outcomes (p = 0.008) at 6 months after carbon monoxide exposure and better improvement of the 6-month Global Deterioration Scale score than the 1-month score (p = 0.006). Our data suggest that in acute severe carbon monoxide poisoning, patients who were treated using therapeutic hypothermia combined with hyperbaric oxygen therapy had significantly more favorable neurocognitive outcomes at 6 months after carbon monoxide exposure than those treated with hyperbaric oxygen therapy alone.

Cardiac injury after acute carbon monoxide poisoning and its clinical treatment scheme.

This study was designed to investigate cardiac injury after acute carbon monoxide poisoning and its clinical treatment scheme. Seventy patients with moderate and severe acute carbon monoxide poisoning (ACOP) admitted from January 2017 to December 2018 into The Affiliated Hospital of Qingdao University were regarded as a research group (RG), and another 30 healthy adults undergoing physical examination in the hospital during the same period were selected as a control group (CG). Thirty-five patients in the RG who received hyperbaric oxygen therapy were considered as group A, and 35 patients who received extracorporeal membrane oxygenation therapy were considered as group B. The effective rates and complications of the two groups after treatment were compared. The concentrations of creatine kinase isoenzyme (CK-MB) and lactate dehydrogenase (LDH) of myocardial enzymes at different time points before and after treatment were detected. Expression of miR-30a in the blood of experimental subjects was detected by time-fluorescence quantitative PCR, and the relationship between miR-30a expression and ACOP patients was analyzed. Patients in groups A and B achieved obvious efficacy, but the effective rate and incidence rate of complications in the extracorporeal membrane oxygenation (ECMO) group were better than those in the hyperbaric oxygen group. The concentrations of CK-MB and LDH in group A and group B were significantly higher than those in control group (P<0.01). The expression level of miR-30a in the RG was significantly higher than that in the control group (P<0.05). Both hyperbaric oxygen therapy and ECMO therapy have obvious efficacy on ACOP patients, but the latter is better than the former. The expression level of miR-30a in blood of ACOP patients increased significantly, which is positively correlated with myocardial injury, and it decreased after treatment. It is believed that miR-30a can provide a reference index for early diagnosis and prediction of disease progression and prognosis in cardiac injury of ACOP.

Application and prospects of butylphthalide for the treatment of neurologic diseases.

ObjectiveThe 3-N-butylphthalide (NBP) comprises one of the chemical constituents of celery oil. It has a series of pharmacologic mechanisms including reconstructing microcirculation, protecting mitochondrial function, inhibiting oxidative stress, inhibiting neuronal apoptosis, etc. Based on the complex multi-targets of pharmacologic mechanisms of NBP, the clinical application of NBP is increasing and more clinical researches and animal experiments are also focused on NBP. The aim of this review was to comprehensively and systematically summarize the application of NBP on neurologic diseases and briefly summarize its application to non-neurologic diseases. Moreover, recent progress in experimental models of NBP on animals was summarized.Data sourcesLiterature was collected from PubMed and Wangfang database until November 2018, using the search terms including “3-N-butylphthalide,” “microcirculation,” “mitochondria,” “ischemic stroke,” “Alzheimer disease,” “vascular dementia,” “Parkinson disease,” “brain edema,” “CO poisoning,” “traumatic central nervous system injury,” “autoimmune disease,” “amyotrophic lateral sclerosis,” “seizures,” “diabetes,” “diabetic cataract,” and “atherosclerosis.”Study selectionLiterature was mainly derived from English articles or articles that could be obtained with English abstracts and partly derived from Chinese articles. Article type was not limited. References were also identified from the bibliographies of identified articles and the authors’ files.ResultsNBP has become an important adjunct for ischemic stroke. In vascular dementia, the clinical application of NBP to treat severe cognitive dysfunction syndrome caused by the hypoperfusion of brain tissue during cerebrovascular disease is also increasing. Evidence also suggests that NBP has a therapeutic effect for neurodegenerative diseases. Many animal experiments have found that it can also improve symptoms in other neurologic diseases such as epilepsy, cerebral edema, and decreased cognitive function caused by severe acute carbon monoxide poisoning. Moreover, NBP has therapeutic effects for diabetes, diabetes-induced cataracts, and non-neurologic diseases such as atherosclerosis. Mechanistically, NBP mainly improves microcirculation and protects mitochondria. Its broad pharmacologic effects also include inhibiting oxidative stress, nerve cell apoptosis, inflammatory responses, and anti-platelet and anti-thrombotic effects.ConclusionsThe varied pharmacologic mechanisms of NBP involve many complex molecular mechanisms; however, there many unknown pharmacologic effects await further study.

The impact of hyperthermia after acute carbon monoxide poisoning on neurological sequelae.

This study investigated whether hyperthermia within the first 24 h after presentation was associated with long-term neurological outcomes after acute carbon monoxide (CO) poisoning. This retrospective study included 200 patients with acute severe CO poisoning. Hyperthermia (≥ 37.5°C) developed during the first 24 h after presentation in 55 (27.5%) patients, and poor long-term neurological sequelae assessed at 23 months after acute CO poisoning developed in 19.5% of the patients. The incidence of poor long-term neurological outcomes was significantly higher in the hyperthermia group than in the normothermia group. Patients with poor long-term neurological outcomes had higher maximum temperatures than patients with good outcomes. No significant difference was found in the time of hyperthermia onset within the first day according to the neurological outcomes. Hyperthermia (adjusted odds ratio (aOR) 5.009 (95% confidence interval (CI) 1.556-16.126)) and maximum temperature (aOR 2.581 (95% CI 1.098-6.063)) within the first 24 h after presentation to the emergency department were independently associated with poor long-term neurological outcomes. Body temperature measurements, which are easily and noninvasively recorded at the bedside in any facility, help to predict the risk for poor long-term neurological outcomes. This study carefully emphasizes fastidious control of pyrexia, particularly during the early period after acute CO poisoning.

The neuroprotective effect of targeted regulation Nrf2 gene on injured brain caused by acute severe carbon monoxide poisoning in rats

Objective To explore the neuroprotective effect of targeted regulation Nrf2 gene on rats with brain injury caused by acute severe carbon monoxide (CO) poisoning. Methods A total of 180 healthy adult SD rats were divided into 4 groups at random: normal control group(NC group), CO poisoning group(CO group), lentivirus group(LV group) and Nrf2 gene therapy group(Nrf2 group), and 45 rats in each group. An acute CO toxic rat model was established by inhalation in a hyperbaric oxygen tank. The lentivirus group was directly injected with lentivirus dilution (4×106 TU/μl) into striatum with a microsyringe guided by a stereotactic apparatus, and the Nrf2 gene therapy group was administrated the same dose of recombinant Nrf2 gene lentivirus dilution, while rats in the normal control group and the CO poisoning group were received the same amount of normal saline. Five rats were taken and decapitated at day 1, day 7 and week 2 from each group, respectively. The mitochondrial membrane potential (MMP) of neurons in brain tissue was detected by JC-1 method, and the expressions of Nrf2 and GCLC proteins were observed by immunohistochemistry and Western Blot. Results Compared with the NC group (cortex: (75.3±6.8); hippocampus: (76.4±7.1); striatum: (73.8±7.3)) at the same time point, the MMPs of neurons in CO group (cortex: (34.5±6.7); hippocampus: (30.3±5.6); striatum: (41.5±6.1) and LV group (cortex: (36.8±6.2); hippocampus: (30.8±6.0); striatum: (42.7±6.3)) were significantly decreased, and the difference was significant(P 0.05). A small amount of Nrf2 protein (0.22±0.05) and GCLC protein (0.24±0.04) were expressed in the brain tissue of normal control rats. The expressions of Nrf2 protein (0.31±0.06, 0.31±0.05) and GCLC protein (0.30±0.04, 0.31±0.07) in CO group and LV group were slightly increased (P 0.05). The MMPs value of nerve cells in the Nrf2 group (cortex: (53.3±5.3); hippocampus: (56.9±6.1); striatum: (60.6±6.0)) also decreased, but it was significantly higher than that in the CO group and the LV group at the same time point (P 0.05). Conclusion CO poisoning could induce oxidative stress and damage mitochondrial function of nerve cells. The active state of targeted regulation Nrf2 could significantly enhance the antioxidant capacity of rats and positively protect rats against brain injury induced by acute severe CO poisoning. Key words: Carbon monoxide poisoning; Brain injury; Mitochondrial membrane potential; Nuclear factor E2 related factor 2

Effect of ulinastatin on myocardial injury in patients with acute severe carbon monoxide poisoning

Objective: To observe the effect of ulinastatin on myocardial injury in patients with acute severe carbon monoxide poisoning (ASCOP) . Methods: By using the prospective study method, 123 cases of ASCOP patients admitted to our hospital, were randomly divided into two groups. There were no significantly different between the two groups in the abnormal rates of ECG, brain natriuretic peptide (BNP) , troponin I (cTNI) , creatine phosphokinase (CK-MB) and creatine phosphokinase (CK) . The control group according to the patients need to be treated with hyperbaric oxygen and routine medical treatment; the observation group was treated with ulinastatin 100 thousand u intravenous injection based on routine treatment measures on Q8 h, the two groups were 7 d for the 1 course of treatment. Compared two groups of patients after 3 days, 7 days of electrocardiogram, brain natriuretic peptide (BNP) , troponin I (cTNI) , creatine kinase isoenzyme (CK-MB) , creatine kinase (CK) , the case fatality rate within 14 days, and the abnormality rate of BNP, cTNI, CK-MB and Ck. Results: the observation group for 3 days, 7 days, 14 days were abnormal, brain natriuretic peptide (BNP) , cardiac troponin I (cTNI) , creatine kinase isoenzyme (CK-MB) , creatine kinase (CK) the average results were significantly lower than those in the control group (P<0.05) ; The 14 d BNP in the observation group was significantly lower than the control group (P<0. 05) ; the case fatality rateof observation group was lower than the control group within 14 days (1.2% vs 3.3%) . Conclusion: Ulinastatin can significantly improve the ASCOP to reduce the damage to the heart, reduce the case fatality rateand improve the prognosis.

Effects of N-butylphthalide on the expressions of calpain 1 and CaMK II in hippocampus in rats with acute severe carbon monoxide poisoning

To investigate the effects of N-butylphthalide (NBP) on cognitive function in acute severe carbon monoxide (CO) poisoning rats and its mechanism. 120 health Sprague-Dawley (SD) rats were randomly divided into three groups (n = 40): normal control group (NC group), CO poisoning group (CO group) and NBP treatment group (NBP group). The acute severe CO poisoning model was established in a hyperbaric oxygen chamber by intoxicated with 1 000 ×10-6 CO for 40 minutes, followed with 3 000 ×10-6 CO for another 20 minutes, and then received hyperbaric oxygen therapy 1.5 hours once a day until sacrificed. Rats in NBP group were administered orally NBP 60 mg/kg for 2 times daily until death. NC group and CO group were treated with equal amount of pure olive oil. Four rats in each group were taken from 1, 3, 7, 14, 30 days after model setup, respectively. The cognitive function score was assessed by Morris water maze test. The changes in ultrastructure of hippocampus were observed under transmission electron microscope. The expressions of calpain 1 and Ca2+/calmodulin dependent protein kinase II (CaMK II) in hippocampus of brain tissue were detected by immunofluorescence staining, and the localization of the two target proteins in neurons was observed by immunofluorescence double staining. Compared with NC group, the escape latency at 1 day after poisoning in CO group was significantly prolonged (s: 55.6±3.2 vs. 44.5±3.5, P < 0.05), and the times of the platform crossing was significantly decreased (times: 1.3±0.8 vs. 6.6±1.2, P < 0.05); the ultrastructure of hippocampus was obviously injured; the protein expressions of calpain 1 and CaMK II in brain tissue were significantly increased at 1 day after CO poisoning [calpain 1 (A value): 41.24±5.21 vs. 6.44±1.13, CaMK II (A value): 56.19±5.04 vs. 9.84±1.53, both P < 0.05], and the protein expression of calpain 1 reached the peak at 3 days (A value: 59.34±6.11), the protein expression of CaMK II reached the peak at 1 day (A value: 56.19±5.04). Compared with CO group, the cognitive function was significantly improved in NBP group in the late stage of poisoning [7-30 days, escape latency (s): 40.3±1.9 vs. 49.1±3.1 at 7 days, 30.1±2.9 vs. 39.4±3.1 at 30 days; times of the platform crossing (times): 2.8±1.0 vs. 1.0±0.9 at 14 days, 3.2±0.8 vs. 1.0±0.9 at 30 days, all P < 0.05]; the degree of injury of hippocampal neuron was relatively slight; the protein expression of calpain 1 in brain tissue was significantly decreased from 3 days after CO poisoning (A value: 39.63±3.03 vs. 59.34±6.11, P < 0.05), and the protein expression of CaMK II was significantly decreased from 1 day after CO poisoning (A value: 42.22±3.84 vs. 56.19±5.04, P < 0.05). Immunofluorescence double staining suggested that calpain 1 and CaMK II protein could not only coexist in the same cell, but also could be expressed separately in different cells. Linear regression analysis showed that the expression of calpain 1 and CaMK II was positively correlated (R 2 = 0.852, P = 0.002). NBP treatment could maintain ultrastructure integrity of hippocampus, balance the expression levels of calpain 1 and CaMK II proteins, and significantly improve cognitive impairment induced by CO poisoning, thus play a protective role against hippocampus damage in rats with acute severe CO poisoning.

Severe pulmonary edema following hyperbaric oxygen therapy for acute carbon monoxide poisoning: a case report and clinical experience

Pulmonary edema following hyperbaric oxygen (HBO₂) therapy is a rare clinical phenomenon. This case report describes such a patient - a 56-year-old woman who suffered from severe pulmonary edema after HBO₂ therapy for carbon monoxide (CO) poisoning. Patient experienced ecphysesis and dyspnea suddenly after HBO₂ therapy (100% oxygen at 0.25 MPa, for 60 minutes with a five-minute air break and decompression at 0.01 MPa/minute). Post therapy her heart rate (HR), blood pressure (BP), respiratory rate (RR) and oxygen saturation (SO₂) were 140 bpm, 60/40 mmHg, 38 bpm and 84%, respectively. Diagnoses of acute pulmonary edema and shock were made. Various treatments including antishock, tracheal intubation, mechanical ventilation for respiratory support, a diuretic, dexamethasone, asthma relief, and acidosis correction were administered. Pulmonary computed tomography (CT) indicated significant pulmonary edema. Due to active treatment, the patient showed gradual improvement. Pulmonary CT re-examination showed pulmonary edema markedly improved. At the two-year follow-up, the patient reported no abnormal mental or neurological symptoms. Acute pulmonary edema is rare but can lead to serious side effects of HBO₂ therapy in patients with severe acute CO poisoning. This complication must be must considered when administering HBO₂ therapy to patients with severe CO poisoning.

Value of early-stage cerebral oxygen utilization coefficient in predicting delayed encephalopathy after acute carbon monoxide poisoning

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.

N-Butylphthalide Improves Cognitive Function in Rats after Carbon Monoxide Poisoning.

Cognitive impairment is the most common neurologic sequelae after carbon monoxide (CO) poisoning, and the previous investigations have demonstrated that N-Butylphthalide (NBP) could exert a broad spectrum of neuroprotective properties. The current study aimed to investigate the effect of NBP on cognitive dysfunction in rats after acute severe CO poisoning. Rats were randomly divided into a normal control group, a CO poisoning group and a CO+NBP group. The animal model of CO poisoning was established by exposure to CO in a chamber, and then all rats received hyperbaric oxygen therapy once daily, while rats in CO+NBP group were administered orally NBP (6 mg/ 100g) by gavage twice a day additionally. The results indicated that CO poisoning could induce cognitive impairment. The ultrastructure of hippocampus was seriously damaged under transmission electron microscopy, and the expressions of calpain 1 and CaMK II proteins were significantly elevated after CO exposure according to the analysis of immunofluorescence staining and western blot. NBP treatment could evidently improve cognitive function, and maintain ultrastructure integrity of hippocampus. The expression levels of both calpain 1 and CaMK II proteins in CO+NBP group were considerably lower than that of CO poisoning group (P < 0.05). Taken together, this study highlights the molecular mechanism of cognitive dysfunction in rats after CO exposure via the upregulation of both calpain 1 and CaMK II proteins. The administration of NBP could balance the expressions of calpain 1 and CaMK II proteins and improve cognitive function through maintaining ultrastructural integrity of hippocampus, and thus may play a neuroprotective role in brain tissue in rats with CO poisoning.

Treatment of acute carbon monoxide poisoning with induced hypothermia.

ObjectiveThe effect of induced hypothermia on severe acute carbon monoxide (CO) poisoning remains to be addressed further. We investigated the effect of induced hypothermia on severe acute CO poisoning.MethodsRetrospective chart review was conducted for patients who diagnosed as severe acute CO poisoning in emergency department and underwent induced hypothermia from May 2013 to May 2014. Hospital courses with critical medication and major laboratory results were investigated through the chart review.ResultsAmong total 227 patients with acute CO poisoning during the period of study, patients with severe acute CO poisoning were 15. All patients underwent induced hypothermia with a temperature goal 33°C. Initial and follow-up levels of S100B protein after induced hypothermia were 0.47 μg/L (interquartile range, 0.11 to 0.71) and 0.10 μg/L (interquartile range, 0.06 to 0.37), respectively (P = 0.01). The mean Glasgow Coma Scales at emergency department admission was 6.87 ± 3.36. Except 1 patient who expired after cardiopulmonary resuscitation, Glasgow Coma Scales at 30-day of hospital discharge were 15 in 10 patients (71.4%), 14 in 1 patient (7.1%), 13 in 1 patient (7.1%), and 6 in 2 patients (14.2%). Seven patients (46.7%) developed delayed neurologic sequelae. Four patients showed mild types of delayed neurologic sequelae and 3 showed moderate to severe types of delayed neurologic sequelae.ConclusionMost of patients underwent induced hypothermia had a good recovery from severe acute CO poisoning. Therefore, induced hypothermia may be considered as a possible treatment in severe acute CO poisoning.

G-CSF administration attenuates brain injury in rats following carbon monoxide poisoning via different mechanisms.

Acute severe carbon monoxide (CO) poisoning induces hypoxia that leads to cardiovascular and nervous systems disturbances. Different complex mechanisms lead to CO neurotoxicity including lipid peroxidation, inflammatory and immune-mediated reactions, myelin degeneration and finally neuronal apoptosis and necrosis. Granulocyte colony-stimulating factor (G-CSF) is considered to be a novel neuroprotective agent. In this study, we evaluated the efficacy of G-CSF therapy on CO neurotoxicity in rats with acute CO poisoning. Rats were exposed to 3000 ppm CO in air (0.3%) for 1 h, and then different doses (50,100, and 150 µg/kg) of G-CSF or normal saline were administrated intraperitoneally. Water content of brain as an indicator for total edema and blood brain barrier integrity (Evans blue extravasation) were evaluated. Malondialydehyde was determined in order to evaluate the effect of G-CSF on CO-induced lipid peroxidation in brain tissues. Also, the effect of G-CSF on myeloperoxidase activity in the brain tissue was evaluated. The effect of G-CSF administration on induced apoptosis in the brain was measured using TUNEL method. To evaluate the level of MBP, STAT3 and pSTAT3 and HO-1 proteins and the effect of G-CSF on these proteins Western blotting was carried out. G-CSF reduced water content of the edematous poisoned brains (100 µg/kg) and BBB permeability (100 and 150 µg/kg) (P < 0.05). G-CSF (150 µg/kg) reduced the MDA level in the brain tissues (P < 0.05 as compared to CO poisoned animals). G-CSF did not decrease the MPO activity after CO poisoning in any doses. G-CSF significantly reduced the number of apoptotic neurons and Caspase 3 protein levels in the brain. Western blotting results showed that G-CSF treatment enhanced expression of HO-1 and MBP, STAT3 and pSTAT3 proteins in the brain tissues. Based on our results, a single dose of G-CSF immediately after CO poisoning significantly attenuates CO neurotoxicity via different mechanisms. © 2015 Wiley Periodicals, Inc. Environ Toxicol 32: 37-47, 2017.