Severe Carbon Monoxide Poisoning Research Articles

Carboxyhemoglobin half-life toxicokinetic profiles during and after normobaric oxygen therapy: On a swine model

Investigations on acute carbon monoxide (CO) poisoning struggle to highlight a relevant discriminant criterion related to CO poisoning severity for predicting complications, such as delayed neurological syndromes. In this context, it remains difficult to demonstrate the superiority of one method of oxygen (O2) administration over others or to identify the optimal duration of normobaric 100% oxygen (NBO) treatment. Myoglobin, as hemoglobin, are a potential binding site for CO, which could be a source of extravascular CO storage that impacts the severity of CO poisoning. It is not possible in routine clinical practice to estimate this potential extravascular CO storage. Indirect means of doing so that are available in the first few hours of poisoning could include, for example, the carboxyhemoglobin half-life (COHbt1/2), which seems to be influenced itself by the level and duration of CO exposure affecting this store of CO within the body. However, before the elimination of CO can be assessed, the COHbt1/2 toxicokinetic model must be confirmed: research still debates whether this model mono- or bi-compartmental. The second indirect mean could be the assessment of a potential COHb rebound after COHb has returned to 5% and NBO treatment has stopped. Moreover, a COHb rebound could be considered to justify the duration of NBO treatment. On an experimental swine model exposed to moderate CO poisoning (940 ppm for ±118 min until COHb reached 30%), we first confirm that the COHb half-life follows a bi-compartmental model. Secondly, we observe for the first time a slight COHb rebound when COHb returns to 5% and oxygen therapy is stopped. On the basis of these two toxicokinetic characteristics in favor of extravascular CO storage, we recommend that COHbt1/2 is considered using the bi-compartmental model in future clinical studies that compare treatment effectiveness as a potential severity criterion to homogenize cohorts of the same severity. Moreover, from a general toxicokinetic point of view, we confirm that a treatment lasting less than 6 hours appears to be insufficient for treating moderate CO poisoning.

Delayed neuropsychiatric syndrome after carbon monoxide poisoning.

Delayed neuropsychiatric syndrome (DNS) is a well-known complication following carbon monoxide (CO) poisoning and develops in up to 50% of adult survivors. The syndrome is probably immunologically mediated. Common symptoms are slowness, Parkinsonism and cognitive impairment. A woman in her forties started to show gradually increasing symptoms of DNS a few days after an episode of severe CO poisoning. She received methylprednisolone 1g intravenously on 3 consecutive days at around 7 weeks after the poisoning, with an immediate positive response to motor deficit symptoms. Thereafter, she gradually recovered and returned to full-time employment 4.5 months after the steroid treatment. The role of steroids in this patient's recovery is uncertain. However, successful high-dose steroid treatment for patients with ongoing DNS progression after CO poisoning has been reported previously in the literature. The authors recommend more attention to the risk of DNS after CO poisoning and further research on treatment options.

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.

Bilateral Hearing Loss after Carbon Monoxide Poisoning

Background: Carbon monoxide (CO) is an odorless, colorless, flammable gas that is formed by the incomplete combustion of fuels and binds to hemoglobin with 200 to 250 times greater affinity compared to oxygen. As a result, blood oxygen-carrying capacity is reduced when CO is bound to hemoglobin. Reversible and irreversible unilateral or bilateral hearing loss due to CO poisoning has rarely been reported. We present a case of an 18-year-old previously healthy male with bilateral hearing loss after severe CO poisoning. Case Report: An 18-year-old male with no past medical history presented to the emergency department (ED) after being found unconscious with emesis in his vehicle. He failed to respond to Naloxone. In the ED, he was obtunded with vital signs significant only for tachycardia of 115 bpm. Initial workup revealed leukocytosis (WBC 16.0 10*3/uL), hyperglycemia (glucose 195 mg/dl ) and high sensitivity troponin elevation (131 ng/L). Electrocardiogram revealed sinus tachycardia with an incomplete right bundle branch block. Head CT and urine drug immunoassay were negative. Several hours after ED arrival, it was reported that the vehicle had a known problem with the exhaust pipe. The patient remained unresponsive for several hours. Approximately 6 hours after ED arrival, a carboxyhemoglobin level was ordered and returned at 9.5%. A non-rebreather oxygen mask was applied and the patient began waking up shortly after. Prior to receiving the first session of hyperbaric oxygen therapy (HBO2), the patient complained of bilateral hearing loss with tinnitus. Three sessions of HBO2 were done in the first 24 hours. The patient remained with bilateral hearing loss and tinnitus with minimal improvement over the three day hospitalization. A 3 day course of dexamethasone 10 mg daily was given. Audiological testing was not performed prior to discharge. Six months after discharge, he continued to have tinnitus and hearing loss though endorsed improvement. His audiogram shows moderate hearing loss. Discussion: CO poisoning is a rare cause of hearing loss. Tinnitus with hearing loss is reported even less. The mechanism for hearing loss in the setting of CO poisoning has not been identified however it is believed to be due to tissue hypoxia. The pattern of hearing loss after acute or chronic CO poisoning is typically sensorineural and could be unilateral or bilateral, reversible or irreversible. HBO2 is commonly used to treat severe CO poisoning, and occasionally to treat idiopathic sensorineural hearing loss (ISNHL). However, HBO2 has not been described for the sole purpose of treating CO-associated hearing loss. Corticosteroids have been shown to prevent delayed neuropsychiatric sequelae after CO poisoning and to treat ISNHL, but no reported cases with CO hearing loss. Due to the potential benefits of these relatively benign interventions, the patient was treated with HBO2 and corticosteroids with improvement in symptoms. Conclusion: Hearing loss is a rare clinical manifestation of carbon monoxide poisoning with few reported cases in the literature. Resulting hearing loss may be unilateral or bilateral, and reversible or irreversible.

Early and late adverse clinical outcomes of severe carbon monoxide intoxication: A cross-sectional retrospective study.

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

The Critical Assessment of Oxidative Stress Parameters as Potential Biomarkers of Carbon Monoxide Poisoning.

In conventional clinical toxicology practice, the blood level of carboxyhemoglobin is a biomarker of carbon monoxide (CO) poisoning but does not correspond to the complete clinical picture and the severity of the poisoning. Taking into account articles suggesting the relationship between oxidative stress parameters and CO poisoning, it seems reasonable to consider this topic more broadly, including experimental biochemical data (oxidative stress parameters) and patients poisoned with CO. This article aimed to critically assess oxidative-stress-related parameters as potential biomarkers to evaluate the severity of CO poisoning and their possible role in the decision to treat. The critically set parameters were antioxidative, including catalase, 2,2-diphenyl-1-picryl-hydrazyl, glutathione, thiol and carbonyl groups. Our preliminary studies involved patients (n = 82) admitted to the Toxicology Clinical Department of the University Hospital of Jagiellonian University Medical College (Kraków, Poland) during 2015-2020. The poisoning was diagnosed based on medical history, clinical symptoms, and carboxyhemoglobin blood level. Blood samples for carboxyhemoglobin and antioxidative parameters were collected immediately after admission to the emergency department. To evaluate the severity of the poisoning, the Pach scale was applied. The final analysis included a significant decrease in catalase activity and a reduction in glutathione level in all poisoned patients based on the severity of the Pach scale: I°-III° compared to the control group. It follows from the experimental data that the poisoned patients had a significant increase in level due to thiol groups and the 2,2-diphenyl-1-picryl-hydrazyl radical, with no significant differences according to the severity of poisoning. The catalase-to-glutathione and thiol-to-glutathione ratios showed the most important differences between the poisoned patients and the control group, with a significant increase in the poisoned group. The ratios did not differentiate the severity of the poisoning. The carbonyl level was highest in the control group compared to the poisoned group but was not statistically significant. Our critical assessment shows that using oxidative-stress-related parameters to evaluate the severity of CO poisoning, the outcome, and treatment options is challenging.

Clinical and Laboratory Characteristics Predicting the Severity of Carbon Monoxide Poisoning in Children: A Single-Center Retrospective Study.

Carbon monoxide poisoning (COP) is extremely common throughout the world. The purpose of this study was to assess the demographic, clinical, and laboratory characteristics predicting the severity COP in children. The study included 380 children diagnosed with COP between January 2017 and January 2021 and 380 healthy controls. Carbon monoxide poisoning was diagnosed based on the medical history and a carboxyhemoglobin (COHb) level of more than 5%. The patients were classified as mild (COHb 10%), moderate (COHb 10%-25%), or severely (COHb > 25%) poisoned. The mean age of the severe group was 8.60 ± 6.30, for the moderate group was 9.50 ± 5.81, for the mild group was 8.79 ± 5.94, and for the control group was 8.95 ± 5.98. The most common place of exposure was at home and all cases were affected accidentally. The coal stove was the most common source of exposure, followed by natural gas. The most common symptoms were nausea/vomiting, vertigo, and headache. Neurologic symptoms such as syncope, confusion, dyspnea, and seizures were more common in the severe group. A total of 91.3% of the children had hyperbaric oxygen therapy, 3.8% were intubated, and 3.8% were transferred to intensive care in the severe group, whereas no death or sequela was observed. Mean platelet volume and red cell distribution width had the highest area under the curve in the receiver operating characteristic analysis (0.659; 0.379). A positive and low statistically significant relationship was found between COHb levels and troponin and lactate levels in the severe group ( P < 0.05). Carbon monoxide poisoning progressed more severely in children presented with neurological symptoms and have elevated red cell distribution width and mean platelet volume. Even in severe COP cases, satisfactory results have been obtained with early and appropriate treatment.

Carbon Monoxide Poisoning Associated Hyperlactatemia

We read with great interest the article titled “TThe Role of SII and SIRI Values in Predicting the Severity of CO Poisoning in the Emergency Department” prepared by Acar and Ertekin, published in the first issue of 2023 of your journal. We thank the authors and the editorial board for the article discussing the relationship between the severity of CO poisoning and combined hematological indices such as systemic immune inflammation index, systemic inflammatory response index and systemic inflammation total index, which have been defined in the last decade in the literature in carbon monoxide (CO) poisoning. However, we would like to point out a few points that will contribute to the discussion of the article on the pathogenesis of hyperlactatemia and the hemodynamic impact in CO poisoning, which the authors used to describe severe poisoning.

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.

Effects of hyperbaric oxygen on Notch signaling pathway after severe carbon monoxide poisoning in mice.

Demyelination of the cerebral white matter is the most common pathological change after carbon monoxide (CO) poisoning. Notch signaling, the mechanism underlying the differentiation of astrocytes and oligodendrocytes, is critical to remyelination of the white matter after brain lesion. The purpose of this work was to determine the effects of hyperbaric oxygen (HBO) on Notch signaling pathway after CO poisoning for the explanation of the protective effects of HBO on CO-poisoning-related cerebral white matter demyelination. The male C57 BL/6 mice with severe CO poisoning were treated by HBO. And HBO therapy shortened the escape latency and improved the body mass after CO poisoning. HBO therapy also significantly suppressed protein and mRNA levels of Notch1 and Hes5 after CO poisoning. Our findings suggested that HBO could suppress the activation of Notch signaling pathway after CO poisoning, which is the mechanism underlying the neuroprotection of HBO on demyelination after severe CO 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.

Истинная степень гемической гипоксии в определении тяжести отравления монооксидом углерода: клиническое наблюдение

Актуальность. Отравление монооксидом углерода является наиболее часто регистрируемой интоксикацией ядовитыми газами. Ранее авторами было выявлено, что наибольшее число отравлений монооксидом углерода в 2015 году произошло по причине пожаров, на втором месте — неисправные системы вентиляции. Цель исследования: улучшение результатов лечения отравления монооксидом углерода посредством более точной диагностики тяжести отравления. Материалы и методы. Анализ клинико-анамнестических и лабораторных данных пострадавших в результате массового отравления монооксидом углерода. С применением показателя «эффективный оксигемоглобин» уточнена степень тяжести отравления. Проведен обзор и анализ доступной литературы, включая данные из базы PubMed. Результаты. Причиной отравления монооксидом углерода послужило нарушение правил эксплуатации бытовой газовой колонки, в результате чего пострадали семь человек (один ребенок госпитализирован в профильный стационар). К значимым клиническим особенностям нами отнесено следующее: относительная тахикардия отмечалась у всех пострадавших, патологические изменения на электрокардиографии выявлены именно у пострадавших с наиболее тяжелой неврологической симптоматикой. В дальнейшем на основании уровня карбоксигемоглобинемии на момент поступления в стационар происходило занижение на один ранг тяжести отравления, установленной клинико-анамнестически. В результате поиска объяснения такого расхождения на основании сведений о повышении сродства гемоглобина к кислороду в условиях карбоксигемоглобинемии авторами предложен расчетный показатель — эффективный оксигемоглобин. После расчета у всех пострадавших эффективный оксигемоглобин соответствовал гемоглобину при анемии легкой степени. Таким образом, применение показателя эффективного оксигемоглобина позволило уточнить тяжесть отравления монооксидом углерода, выявленную лабораторно, что повысило обоснованность клинико-анамнестической оценки. Выводы. При определении тяжести отравления монооксидом углерода ранняя оценка истинной степени гемической гипоксии посредством показателя эффективного оксигемоглобина позволит повысить обоснованность прогноза заболевания и улучшить результаты лечения таких пострадавших.

Carbon monoxide: modern concepts to the treatment of acute poisonings (literature review)

Introduction. Carbon monoxide (CO) is one of the most common causes of chemical injuries and the main toxic factor in the people death in fires. The mechanism of the toxic effect of CO, associated with the formation of carboxyhemoglobin and the development of hypoxia, determines the rapid development of the clinical picture of acute intoxication and the need for emergency first aid and medical care to the poisoned. Material and methods. Literature sources, summarized in the bibliographic databases eLIBRARY.RU, PubMed and Scopus, were the material for analysis. Results. First aid is based on quickly removing the victim from the fire zone or other area with a high concentration of CO and providing him with oxygen as soon as possible. During medical evacuation, it is necessary to carry out continuous inhalation of 80-100% oxygen, to ensure rest and warmth of the victim. In the emergency department of the hospital, oxygen inhalation and maintenance therapy should be continued, clinical and laboratory diagnostic measures aimed at assessing the severity of intoxication, identifying complications and concomitant pathology should be performed. In the case of severe CO poisoning, medical care continues to be provided to the victims in the intensive care unit or in the oxygen-barotherapy unit. The main antidote for CO poisoning is oxygen, which can be used in two versions - normobaric or hyperbaric oxygenation. As a pharmacological antidote to CO, zinc bisvinylimidazole diacetate (acizol) which can accelerate the breakdown of carboxyhemoglobin, improve the oxygen-binding and gas-transport properties of blood, as well as the dissociation of oxyhemoglobin in tissues is used. Along with antidotes, an important role in the treatment of CO poisoning is played by pathogenetic and symptomatic therapy aimed at the prevention and treatment of toxic encephalopathy, brain edema, cognitive dysfunction, toxic myocardiodystrophy and arrhythmia, prevention of pneumonia, correction of the acid-base state, compensation of the energy needs of the body, etc. Conclusion. Further improvement of existing means and methods for the treatment of intoxication, the development and introduction of new antidots into medical practice will increase the effectiveness of therapeutic measures, reduce the number of deaths and disabilities after acute poisoning with carbon monoxide.

Risk of acute kidney injury among patients with carbon monoxide poisoning.

There is a lack of evidence supporting the association between carbon monoxide (CO) poisoning and acute kidney injury (AKI). Hence, the present study aimed to evaluate the association between CO poisoning and AKI.From 2000 to 2011, we identified patients diagnosed with CO poisoning from the inpatient claims data. Patients aged below 20 years, who had a history of chronic kidney disease or end-stage renal disease before the index date and had incomplete medical information were excluded. Control patients without CO poisoning were randomly selected from all National Health Insurance beneficiaries, and the same exclusion criteria were used. The control group was frequency matched to patients with CO poisoning based on age, sex, and year of CO poisoning diagnosis. Cox proportional hazards regression analyses were conducted to assess the effects of CO poisoning on the risk of AKI. The hazard ratios and 95% confidence interval (CI) were calculated in the models.Compared with the control cohort, patients with severe CO poisoning were 3.77 times more likely to develop AKI (95% CI = 2.20-6.46), followed by those with less severe CO poisoning (adjusted hazard ratio = 2.21, 95% CI = 1.61-3.03).The findings of this nationwide study suggest an increased risk of AKI in patients with CO poisoning.

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.

Evaluation of the Cardioprotective Effect of Granulocyte Colony Stimulating Factor in Patients with Carbon Monoxide Poisoning.

Carbon monoxide (CO), which is well known as silent killer, has many toxic effects on organs with high rate of metabolism such as heart and brain. CO-induced cardiotoxicity resulted in a wide range of disabilities including electrocardiogram (ECG) abnormalities, elevation in level of cardiac enzymes, arrhythmias, impairment of left ventricular and myocardial infarction (MI). Cardio-protective effects of Granulocyte colony-stimulating factor (G-CSF) on infarcted heart was proved previously in various reports. In this study, possible effect of G-CSF on cardiac function of patients with moderate to severe acute CO poisoning was investigated. Cardioprotective effects of G-CSF in CO-poisoned patients was evaluated through ECG, Holter monitoring, echocardiography, and biochemical studies. Continuous intravenous infusion of G-CSF (90 μg/kg) and normal saline were administered respectively to treatment and placebo groups. The results demonstrated that in moderate to severe CO poisoning, myocardial injury is common. ECG changes (e.g., ST-segment and T-wave changes, QTC), cardiac arrhythmias (e.g., heart blocks and ventricular arrhythmias), serum level of Troponin I, left ventricular ejection fraction were determined after G-CSF administration. Frequencies of ST depression, inversion or flatting of T wave and QTC in ECG were significantly reduced after G-CSF treatment. In addition, incidence of cardiac arrhythmias due to CO poisoning were reduced after G-CSF treatment. However, G-CSF did not exert protective effects on TPI level and function of left ventricular in CO-poisoned patients. GCSF could probably reduce CO-induced cardiac ischemia in patients with acute CO poisoning. The trial protocol was registered in the Iranian Registry of Clinical Trials (http://www.irct.ir) registry (Irct ID: IRCT201607232083N7).

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.

The Value of Neutrophil:Lymphocyte Ratio and Platelet:Lymphocyte Ratio in Predicting Clinical Severity in Children with Carbon Monoxide Poisoning.

To compare the values of neutrophil:lymphocyte ratio (NLR), platelet:lymphocyte ratio (PLR), and mean platelet volume (MPV) with carboxyhemoglobin (COHb) and lactate levels in children with acute CO intoxication. In this retrospective study, the patients were divided into two groups: mild-to-moderate carbon monoxide poisoning (COP) (COHb 10%-20%) and severe COP (COHb >20%) according to the COHb levels in the application. All patients were compared in terms of NLR, PLR, and MPV parameters according to the severity of poisoning and the high lactate levels (≥ 2.2mmol/L). A total of 261 children with COP were included in the study. The number of patients with mild-to-moderate COP was 183 (70.1%), and the number of patients with severe COP was 78 (29.9%). NLR [2.57 (3.27), 1.65 (1.93), (p = 0.001)] and PLR [123.0 (88.24), 92.8 (54.1), (p = 0.001)] values of mild-to-moderate COP were statistically significantly lower than the severe COP group. In the group with high lactate level, PLR values were significantly lower [120.1 (71.9), 100.2 (85.4), (p = 0.017)]. NLR and PLR values were found to be predictive of severe COP. NLR and PLR can be used for detection of clinical severity in patients with COP. PLR can be used in conjunction with lactate levels to detect tissue-level exposure in patients with COP.