Acute Carbon Monoxide Research Articles

Correlation between Time to Hyperbaric Oxygen Therapy and Delayed Neurological Sequelae in Acute Carbon Monoxide Poisoning Patients.

Carbon monoxide (CO) is one of the most common causes of intoxication. Delayed neurologic sequelae (DNS) have a major impact on prognosis of CO poisoning patients. Hyperbaric oxygen therapy (HBOT) is widely used to treat DNS. However, there is no consensus regarding the optimal timing of HBOT. This prospective study enrolled patients who visited the hospital from November 2019 to October 2022. The cutoff value for the latency to HBOT after CO exposure was determined, and the area under the receiver operating characteristic curve (AUC) was estimated. In total, 167 patients were divided into non-DNS and DNS groups. The initial Glasgow Coma Scale (GCS) score, CO exposure time, latency to HBOT after CO exposure, median length of hospital stay (p < 0.001) and creatine kinase (p = 0.016) showed significant differences. A GCS score ≤ 9 had an odds ratio (OR) of 5.059 (95% confidence interval [CI]: 1.602-15.976, p = 0.006), and latency to HBOT after CO exposure ≥ 200 min had an OR of 18.971 (95% CI: 4.310-83.508, p < 0.001). The AUC was 0.8235 (95% CI: 0.7504-0.8966). A GCS score ≤ 9 and latency to HBOT ≥ 200 min may be significant risk factors for DNS.

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.

Changes of Nuclear Factor Kappa-B Pathway Activity in Hippocampus After Acute Carbon Monoxide Poisoning and Its Role in Nerve Cell Injury.

Acute carbon monoxide poisoning (ACOP) causes tissue hypoxia and damage mainly by binding to hemoglobin (Hb). This article aimed to explore the changes in the activity of nuclear factor kappa-B (NF-κB) pathway in the hippocampus after ACOP and its role in nerve cell damage. This article used 30 Sprague-Dawley (SD) rats as the research object, which were randomly divided into two groups, ACOP group and controls. The model of carbon monoxide (CO) poisoning was established, and then the activity of NF-κB pathway in the hippocampus of the two groups of rats was detected, and the statistical analysis was performed. Compared with the controls, the activity of NF-κB pathway in the hippocampus of the ACOP group was significantly increased (P < 0.05). The degree of neuronal damage in the ACOP group was also significantly increased. ACOP increases the activity of the NF-κB pathway in the hippocampus and may cause neuronal damage through this pathway. This provides new ideas and methods for the treatment of ACOP, and also provides new evidence for the role of NF-κB pathway in neuronal injury.

Stroke on ECG: a cerebral T-wave change secondary to acute carbon monoxide poisoning

In clinical management of carbon monoxide (CO) poisoning, serum cardiac enzyme biomarkers and electrocardiogram (ECG) are both highly recommended emergency check-ups to evaluate myocardial injuries. Medical imaging – including head CT or MRI – are not routine for CO poisoning emergency management. We herein report on a comatose patient who was diagnosed with cerebral infarction secondary to 24 hours previous acute CO poisoning, warned by a typical cerebral-type T waves on ECG in advance, and confirmed by a head MRI. Fortunately, the patient made a full recovery based on a timely treatment with medications and hyperbaric oxygen (HBO2) therapy. We would like to propose that a vital, stable, conscious CO poisoning patient who remains a higher risk for hemorrhagic or ischemic stroke should be closely monitored for potential neurological abnormalities, and a continuous ECG monitoring should be reinforced throughout the treatment. A head MRI or CT is a priority in evaluating the secondary cerebral stroke and should be arranged immediately in the event of an abnormal ECG or if unusual new symptoms are apparent. Keywords: carbon monoxide poisoning; cerebral infarction; cerebral T-wave; magnetic resonance imaging (MRI)

Patterns of carbon monoxide poisoning and its association with delayed neuropsychiatric sequela at a tertiary hospital in Riyadh, Saudi Arabia.

Background: Carbon Monoxide (CO) is one of the most common environmental causes of acute intoxication globally. It occurs due to impaired tissue oxygenation which has a detrimental impact on systems with high oxygen demands such as cardiovascular and neurological systems. It can lead to Delayed Neuropsychiatric Sequelae (DNS) which may develop in 2-40 days after remission of acute CO poisoning. DNS is defined by recurrent-transient neurological, cognitive, or psychological manifestations. This study was intended to explore the development of DNS for patients exposed to CO intoxication in Saudi Arabia. Methods: A retrospective descriptive cross-sectional study was conducted in subjects who were diagnosed with CO poisoning at King Abdulaziz Medical City (KAMC) and King Abdullah Specialist Children&amp;apos;s Hospital (KASCH) in Riyadh during the period from January 2016 to December 2021. Patient demographics, vitals, diagnostic tests, and oxygen therapy at initial presentation were documented. Patient medical records were reviewed at 2-40 days following CO poisoning for development of DNS. The type of developed DNS and the onset time were also documented. Ethical approval was obtained from King Abdullah International Medical Research Center (KAIMARC). Results: A total of 85 patients were diagnosed with CO poisoning and met the study inclusion criteria. Of these, 76% were adults with an average age of 32.36 (SD± 15.20) and 51% were male adults. The majority of the incidents occurred in the winter season (76%), especially in enclosed spaces (84%). 25% of the patients were smokers. Of those 85 patients, only 5 (6%) developed DNS. Common symptoms included dizziness, nausea, and decreased visual acuity in 40% of the cases. The development of DNS manifestations was most likely (80%) to occur at two to ten days after the initial incident. Inferential statistics showed that BMI (p-value = 0.021) and age group (p-value = 0.029) were significantly associated with COHb level, which was not the case for gender and the presence of clinical manifestation. Furthermore, there was no statistically significant association between gender, age, BMI, gender, type of exposure, presence of clinical manifestations, and COHb level with the development of DNS. Only one reported death in this study. Conclusion: The findings of this study showed that few patients who were exposed to CO poisoning have developed DNS. BMI and age group were significantly associated with COHb level. Further larger-scale multicenter studies are needed to assess the factors associated with the development of DNS for patients with CO poisoning.

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.

Choline as a specific manifestation of delayed encephalopathy after acute carbon monoxide poisoning: a description of two cases.

Choline as a specific manifestation of delayed encephalopathy after acute carbon monoxide poisoning: a description of two cases.

Comparison of hyperbaric oxygen therapy pressures for acute carbon monoxide poisoning

Purpose: No consensus currently exists regarding the maximal pressure of hyperbaric oxygen (HBO&lt;sub&gt;2&lt;/sub&gt;) therapy performed within 24 hours of acute carbon monoxide (CO) poisoning. This study aimed to evaluate the difference in therapeutic effects according to the first HBO&lt;sub&gt;2&lt;/sub&gt; pressure (3.0 atmospheres absolute [ATA] vs. 2.8 ATA).Methods: We used prospectively collected registry data on CO poisoning at a tertiary academic hospital in the Republic of Korea. Adult patients with acute CO poisoning treated with HBO&lt;sub&gt;2&lt;/sub&gt; within 24 hours after arrival at the emergency department and without the use of additional HBO&lt;sub&gt;2&lt;/sub&gt; after 24 hours between January 2007 and February 2022 were included. Data from 595 patients were analyzed using propensity score matching (PSM). Patients with mild (non-intubated) and severe (intubated) poisoning were also compared. Neurocognitive outcomes at 1 month after CO poisoning were evaluated using the Global Deterioration Scale combined with neurological impairment.Results: After PSM, the neurocognitive outcomes at 1-month post-CO exposure were not significantly different between the 2.8 ATA (110 patients) and 3.0 ATA (55 patients) groups (&lt;i&gt;p&lt;/i&gt;=1.000). Similarly, there was also no significant difference in outcomes in a subgroup analysis according to poisoning severity in matched patients (165 patients) (mild [non-intubated]: &lt;i&gt;p&lt;/i&gt;=0.053; severe [intubated]: &lt;i&gt;p&lt;/i&gt;=1.000).Conclusion: Neurocognitive sequelae at 1 month were not significantly different between HBO&lt;sub&gt;2&lt;/sub&gt; therapy pressures of 2.8 ATA and 3.0 ATA in patients with acute CO poisoning. In addition, the 1-month neurocognitive sequelae did not differ significantly between intubated and non-intubated patients.

Changes in the characteristics of acute carbon monoxide poisoning patients who visited the emergency department during the COVID-19 pandemic

Purpose: This study investigated the differences between patients with acute carbon monoxide (CO) poisoning who visited the emergency department (ED) before and during the coronavirus disease 2019 (COVID-19) pandemic.Methods: This was a single-center retrospective observational study. Patients with CO poisoning who visited the ED during the period from February 2020 to January 2023 were classified as the COVID-19 pandemic group, and those from February 2019 to January 2020 were classified as the non-pandemic group. Patients’ medical records were reviewed, their demographic and clinical characteristics were compared, and the length of stay in ED was checked. The time from admission to the ED to the start of hyperbaric oxygenation (HBO) was defined as the door-to-HBO time, and this parameter was compared between both groups.Results: In total, 672 patients were included in this study. The proportion of intentional poisoning was significantly higher in the COVID-19 pandemic group than in the non-pandemic group (&lt;italic&gt;p&lt;/italic&gt;=0.028). The proportion of intentional poisoning significantly increased in the 20- to 29-year-old age group during the COVID-19 pandemic (&lt;italic&gt;p&lt;/italic&gt;&lt;0.001). In addition, it took longer to initiate HBO in the COVID-19 pandemic group than in the non-pandemic group (&lt;italic&gt;p&lt;/italic&gt;=0.001).Conclusion: These findings suggest that pandemics of infectious diseases, such as COVID-19, increase the proportion of intentional CO poisoning, and it may take longer to initiate HBO after visiting the ED. Efforts will be needed to decrease intentional CO poisoning and length of stay in ED.

Clinical and Echocardiographic Predictors for the Presence of Late Gadolinium Enhancement on Cardiac Magnetic Resonance Imaging in Patients with Carbon Monoxide Poisoning.

Late gadolinium enhancement (LGE) on cardiac magnetic resonance imaging (CMRI) reflects the burden of myocardial damage in carbon monoxide (CO) poisoning. This study aimed to identify the clinical and echocardiographic parameters that can predict myocardial LGE on CMRI in CO poisoning. This prospective observational study included patients who presented with acute CO poisoning and elevated troponin I and underwent echocardiography and CMRI to identify myocardial damage at a tertiary university hospital between August 2017 and May 2019 and August 2020 and July 2022. Based on the CMRI findings, participants were categorized into LGE and non-LGE groups. The median age of the 155 patients was 51.0 years, and 98 (63.2%) were males. Median times from emergency department arrival to either CMRI or echocardiography were 3.0 days each. The LGE group included 99 (63.9%) patients with LGE positivity on CMRIs. Time from rescue to hyperbaric oxygen therapy >4 h (odds ratio (OR): 3.31, 95% confidence interval (CI): 1.28-8.56, p = 0.01); serum lactate levels >2 mmol/L (OR: 2.62, 95% CI: 1.20-5.73, p = 0.02); and left ventricular global longitudinal strain >-16% (OR: 2.95, 95% CI: 1.35-6.47, p = 0.007) were significant predictors of LGE positivity. The area under the curve of these predictors was 0.711. Our prediction model, which combines the clinical parameters with left ventricular global longitudinal strain, may be helpful in the early detection of LGE positivity.

Predicting acute brain lesions on magnetic resonance imaging in acute carbon monoxide poisoning: a multicenter prospective observational study

An acute brain lesion (ABL) identified by brain magnetic resonance imaging (MRI) after acute carbon monoxide (CO) poisoning is a strong prognostic factor for the development of delayed neuropsychiatric syndrome (DNS). This study aimed to identify predictors of ABLs on MRI in patients with acute CO poisoning. This was a multicenter prospective registry-based observational study conducted at two tertiary hospitals. A total of 1,034 patients were included. Multivariable logistic regression analysis showed that loss of consciousness (LOC) (adjusted odds ratio [aOR] 2.68, 95% Confidence Interval [CI]: 1.49–5.06), Glasgow Coma Scale (GCS) score < 9 (aOR 2.41, 95% CI: 1.49–3.91), troponin-I (TnI) (aOR 1.22, 95% CI: 1.08–1.41), CO exposure duration (aOR 1.09, 95% CI: 1.05–1.13), and white blood cell (WBC) (aOR 1.05, 95% CI: 1.01–1.09) were independent predictors of ABLs on MRI. LOC, GCS score, TnI, CO exposure duration, and WBC count can be useful predictors of ABLs on MRI in patients with acute CO poisoning, helping clinicians decide the need for an MRI scan or transfer the patient to an appropriate institution for MRI or hyperbaric oxygen therapy.

Effect of hyperbaric oxygen on symptoms of dementia in patients with delayed encephalopathy after acute carbon monoxide poisoning.

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

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

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. 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. 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. 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.

Effect and molecular mechanism of Sulforaphane alleviates brain damage caused by acute carbon monoxide poisoning:Network pharmacology analysis, molecular docking, and experimental evidence.

Sulforaphane (SFN) has attracted much attention due to its ability on antioxidant, anti-inflammatory, and anti-apoptotic properties, while its functional targets and underlying mechanism of action on brain injury caused by acute carbon monoxide poisoning (ACOP) have not been fully elucidated. Herein, we used a systematic network pharmacology approach to explore the mechanism of SFN in the treatment of brain damage after ACOP. In this study, the results of network pharmacology demonstrated that there were a total of 81 effective target genes of SFN and 36 drug-disease targets, which were strongly in connection with autophagy-animal signaling pathway, drug metabolism, and transcription disorders in cancer. Upon the further biological function and KEGG signaling pathway enrichment analysis, a large number of them were involved in neuronal death, reactive oxygen metabolic processes and immune functions. Moreover, based on the results of bioinformatics prediction associated with multiple potential targets and pathways, the AMP-activated protein kinase (AMPK) signaling pathway was selected to elucidate the molecular mechanism of SFN in the treatment of brain injury caused by ACOP. The following molecular docking analysis also confirmed that SFN can bind to AMPKα well through chemical bonds. In addition, an animal model of ACOP was established by exposure to carbon monoxide in a hyperbaric oxygen chamber to verify the predicted results of network pharmacology. We found that the mitochondrial ultrastructure of neurons in rats with ACOP was seriously damaged, and apoptotic cells increased significantly. The histopathological changes were obviously alleviated, apoptosis of cortical neurons was inhibited, and the number of Nissl bodies was increased in the SFN group as compared with the ACOP group (p < .05). Besides, the administration of SFN could increase the expressions of phosphorylated P-AMPK and MFN2 proteins and decrease the levels of DRP1, Caspase3, and Casapase9 proteins in the brain tissue of ACOP rats. These findings suggest that network pharmacology is a useful tool for traditional Chinese medicine (TCM) research, SFN can effectively inhibit apoptosis, protect cortical neurons from the toxicity of carbon monoxide through activating the AMPK pathway and may become a potential therapeutic strategy for brain injury after ACOP.

Investigation of Cerebral Mitochondrial Injury in a Porcine Survivor Model of Carbon Monoxide Poisoning.

Carbon monoxide (CO) is a colorless and odorless gas that is a leading cause of environmental poisoning in the USA with substantial mortality and morbidity. The mechanism of CO poisoning is complex and includes hypoxia, inflammation, and leukocyte sequestration in brain microvessel segments leading to increased reactive oxygen species. Another important pathway is the effects of CO on the mitochondria, specifically at cytochrome c oxidase, also known as Complex IV (CIV). One of the glaring gaps is the lack of rigorous experimental models that may recapitulate survivors of acute CO poisoning in the early phase. The primary objective of this preliminary study is to use our advanced swine platform of acute CO poisoning to develop a clinically relevant survivor model to perform behavioral assessment and MRI imaging that will allow future development of biomarkers and therapeutics. Four swine (10kg) were divided into two groups: control (n = 2) and CO (n = 2). The CO group received CO at 2000ppm for over 120min followed by 30min of re-oxygenation at room air for one swine and 150min followed by 30min of re-oxygenation for another swine. The two swine in the sham group received room air for 150min. Cerebral microdialysis was performed to obtain semi real-time measurements of cerebral metabolic status. Following exposures, all surviving animals were observed for a 24-h period with neurobehavioral assessment and imaging. At the end of the 24-h period, fresh brain tissue (cortical and hippocampal) was immediately harvested to measure mitochondrial respiration. While a preliminary ongoing study, animals in the CO group showed alterations in cerebral metabolism and cellular function in the acute exposure phase with possible sustained mitochondrial changes 24h after the CO exposure ended. This preliminary research further establishes a large animal swine model investigating survivors of CO poisoning to measure translational metrics relevant to clinical medicine that includes a basic neurobehavioral assessment and post exposure cellular measures.

Targeting Ferroptosis Promotes Functional Recovery by Mitigating White Matter Injury Following Acute Carbon Monoxide Poisoning.

Survivors experiencing acute carbon monoxide poisoning (ACMP) tend to develop white matter injury (WMI). The mechanism of ACMP-induced WMI remains unclear. Considering the role of ferroptosis in initiating oligodendrocyte damage to deteriorate WMI, exploring therapeutic options to attenuate ferroptosis is a feasible approach to alleviating WMI. Our results indicated that ACMP induced accumulation of iron and reactive oxygen species (ROS) eventually leading to WMI and motor impairment after ACMP. Furthermore, ferrostatin-1 reduced iron and ROS deposition to alleviate ferroptosis, thereafter reducing WMI to promote the recovery of motor function. The nuclear factor erythroid-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) signaling pathway was found to be involved in alleviating ferroptosis as seen with the administration of ferrostatin-1. The present study rationalizes that targeting ferroptosis to alleviate WMI is a feasible therapeutic strategy for managing ACMP.

Carbon Monoxide Poisoning: From Microbes to Therapeutics.

Carbon monoxide (CO) poisoning leads to 50,000-100,000 emergency room visits and 1,500-2,000 deaths each year in the United States alone. Even with treatment, survivors often suffer from long-term cardiac and neurocognitive deficits, highlighting a clear unmet medical need for novel therapeutic strategies that reduce morbidity and mortality associated with CO poisoning. This review examines the prevalence and impact of CO poisoning and pathophysiology in humans and highlights recent advances in therapeutic strategies that accelerate CO clearance and mitigate toxicity. We focus on recent developments of high-affinity molecules that take advantage of the uniquely strong interaction between CO and heme to selectively bind and sequester CO in preclinical models. These scavengers, which employ heme-binding scaffolds ranging from organic small molecules to hemoproteins derived from humans and potentially even microorganisms, show promise as field-deployable antidotes that may rapidly accelerate CO clearance and improve outcomes for survivors of acute CO poisoning.

Serum neurofilament light chain for predicting delayed neurological sequelae after acute carbon monoxide poisoning.

Acute carbon monoxide (CO) poisoning survivors may experience persistent delayed neurological sequelae (DNS). No studies have investigated the serum neurofilament light chain (NFL) as a prognostic biomarker in acute CO poisoning. This study aimed to determine the serum NFL levels to predict the DNS after acute CO poisoning. Patients with acute CO poisoning who were consecutively admitted from October 2020 to September 2022 were included. The predictive performance of NFLs for the DNS was assessed through the analyses of the correlation, the logistic regression, and the receiver operating characteristic (ROC) curve. Overall, 9.7% (15/155) of the patients had DNS. The serum NFLs in patients with DNS was 113.7pg/mL, which is significantly higher than that in the non-DNS group (25.8pg/mL; P < 0.001). Correlation analysis shows that the serum NFLs are positively correlated with DNS (r = 0.567, P < 0.001). After multiple adjustments, the serum NFLs are independently correlated with DNS [adjusted odds ratio1.032; 95% confidence interval (CI)1.001, 1.064; p = 0.043]. The ROC curve indicates an area under the curve (AUC) of 0.923 (95% CI0.869, 0.960), with a sensitivity of 100% and a specificity of 84.3% at the best cutoff value of 73.4pg/mL. Pairwise comparison shows that the AUC of the NFL is significantly higher than that of the neuron specific enolase (AUC = 0.779) using the Hanley and McNeil test (Z = 2.283, p = 0.022). Serum NFL could be a biomarker of the DNS after acute CO poisoning.

The Possible Role of Partial Pressure of Carbon dioxide Level Changes in the Outcome of Acute Carbon Monoxide Poisoning

The Possible Role of Partial Pressure of Carbon dioxide Level Changes in the Outcome of Acute Carbon Monoxide Poisoning

Hyperbaric oxygenation improve red blood cell deformability in patients with acute or chronic inflammation.

Red blood cells (RBC) are one of the key elements of the microcirculation. Their ability to pass through capillaries and to deliver oxygen to cells is due to their large degree of deformability linked to the characteristics of the RBC membrane. Alterations in RBC deformability as a result of membrane damage, linked in part to increased synthesis of reactive oxygen species (ROS), can be observed in several diseases, such as sepsis, and may contribute to the altered microcirculation observed in these pathologies. Hyperbaric oxygen therapy (HBOT), with inhalation of 100% oxygen, has been proposed in several acute or chronic pathologies, including carbon monoxide poisoning. We investigated the effects of HBOT on oxidative stress from ROS produced by myeloperoxidase (MPO) and on RBC deformability in patients with acute or chronic inflammation (n=10), in patients with acute carbon monoxide poisoning (n=10), and in healthy volunteers (n=10). RBC deformability was evaluated before and after HBOT in the various populations using the ektacytometry technique (Laser-assisted Optical Rotational Red Cell Analyzer - LORRCA). Deformability was determined by the elongation index (EI) in relation to the shear stress (SS) over a range of 0.3 to 50Pa. Oxidative stress was estimated through changes in proteins (chlorotyrosine and homocitrulline) induced by MPO activity measured by liquid chromatography-tandem mass spectrometry analysis. Before HBOT, EI was significantly lower in patients with acute or chronic inflammation than in healthy volunteers and patients with acute carbon monoxide poisoning for the majority of SS values studied. After one session of HBOT, the EI was significantly higher than before HBOT for SS values of 1.93Pa or higher in patients with acute or chronic inflammation. This effect remains constant after 10 sessions. There were no differences before and after HBOT in protein or amino acid oxidation due to ROS generation mediated by MPO in the three populations. Our results confirm altered RBC deformability in patients with acute and chronic conditions associated with an underlying inflammatory process. HBOT improves deformability only after one session and therefore may improve microcirculation in this population. According to our results, this improvement does not seem mediated by the ROS pathway via MPO. These results need to be confirmed in a larger population.