Effects Of Carbon Monoxide Poisoning Research Articles

Effect of Carbon Monoxide Poisoning on Epilepsy Development: A Nationwide Population-Based Cohort Study.

Carbon monoxide (CO) poisoning causes central nervous system toxicity resulting in delayed neurologic sequelae. This study aims to evaluate the risk of epilepsy in patients with a history of CO intoxication. We conducted a retrospective population-based cohort study using the Taiwan National Health Insurance Research Database and enrolled patients with and without CO poisoning matched for age, sex, and index year in a 1:5 ratio, between 2000 and 2010. Multivariable survival models were used to assess the risk of epilepsy. The primary outcome was newly developed epilepsy after the index date. All patients were followed until a new diagnosis of epilepsy, death, or December 31, 2013. Stratification analyses by age and sex were also conducted. This study included 8,264 patients with CO poisoning and 41,320 without. Patients with a history of CO poisoning were strongly associated with subsequent epilepsy (adjusted hazard ratio [HR] 8.40; 95% confidence interval [CI], 6.48 to 10.88). In the age-stratified analysis, intoxicated patients aged 20 to 39 years had the highest HR (adjusted HR 11.06; 95% CI, 7.17 to 17.08). In the sex-stratified analysis, adjusted HRs for male and female patients were 8.00 (95% CI, 5.86 to 10.92) and 9.53 (95% CI, 5.95 to 15.26), respectively. Patients with CO poisoning were associated with an increased risk of developing epilepsy compared with those without CO poisoning. This association was more prominent in the young population.

What is New in Eurasian Journal of Emergency Medicine-Long-term Cardiac Effect of Carbon Monoxide Poisoning

What is New in Eurasian Journal of Emergency Medicine-Long-term Cardiac Effect of Carbon Monoxide Poisoning

The Investigation of Air Pollution for Carbon Monoxide Evaluations in Guatemala City

Carbon Monoxide (CO) is a common gas released naturally and due to industrialization. When released into the air, this gas is one of the most dangerous factors of air pollution, which harms the environment and human health. In third-world countries such as Guatemala, Honduras, and India, people face severe illnesses, including carbon monoxide poisoning, respiratory diseases, and premature deaths due to air pollution, mainly occurring during the rapid urbanization of major cities. This urbanization and increasing number of motor vehicles affect the high levels of CO, which results in deaths from various respiratory diseases. Despite the harmful effects of CO poisoning, significant actions have yet to be taken. Therefore, the research team has been taken to Guatemala City, Guatemala's most populated city, to measure Carbon Monoxide levels in various locations under various conditions.
 An Easy Log USB has been used to measure Carbon Monoxide (CO) levels to assess the areas with a high level of harmful CO. The study has found that an enormous amount of CO is present in highly populated areas, 100 ~ 200% up for a certain time, compared to the indoor air, and reached a result that corroborated the assertions that CO poisoning with 20% higher CO in their hemoglobin might increase the number of intoxicated Guatemalan people. The national government should implement appropriate regulations and methods to follow up on CO emissions and reduce its consequence to prosper economically and socially.

Cascading effects of disaster-related CO exposures during pregnancy

Disaster-related carbon monoxide (CO) poisoning can occur in the event of extended power loss and subsequent use of makeshift heating and cooking elements in poorly ventilated spaces. The maternal-fetal dyad represents populations highly vulnerable to disasters and the subsequent compounding effects of CO poisoning. This study synthesizes evidence related to disaster-associated global CO exposures, reports of CO exposures in pregnancy, and associated individual outcomes in the maternal-fetal dyad. Implications related to UNDRR include Sendai Priorities I and IV: understanding associated risks and disaster risk reduction strategies to reduce the incidence of CO poisoning in vulnerable populations.

A neuroglobin-based high-affinity ligand trap reverses carbon monoxide–induced mitochondrial poisoning

Carbon monoxide (CO) remains the most common cause of human poisoning. The consequences of CO poisoning include cardiac dysfunction, brain injury, and death. CO causes toxicity by binding to hemoglobin and by inhibiting mitochondrial cytochrome c oxidase (CcO), thereby decreasing oxygen delivery and inhibiting oxidative phosphorylation. We have recently developed a CO antidote based on human neuroglobin (Ngb-H64Q-CCC). This molecule enhances clearance of CO from red blood cells in vitro and in vivo Herein, we tested whether Ngb-H64Q-CCC can also scavenge CO from CcO and attenuate CO-induced inhibition of mitochondrial respiration. Heart tissue from mice exposed to 3% CO exhibited a 42 ± 19% reduction in tissue respiration rate and a 33 ± 38% reduction in CcO activity compared with unexposed mice. Intravenous infusion of Ngb-H64Q-CCC restored respiration rates to that of control mice correlating with higher electron transport chain CcO activity in Ngb-H64Q-CCC-treated compared with PBS-treated, CO-poisoned mice. Further, using a Clark-type oxygen electrode, we measured isolated rat liver mitochondrial respiration in the presence and absence of saturating solutions of CO (160 μm) and nitric oxide (100 μm). Both CO and NO inhibited respiration, and treatment with Ngb-H64Q-CCC (100 and 50 μm, respectively) significantly reversed this inhibition. These results suggest that Ngb-H64Q-CCC mitigates CO toxicity by scavenging CO from carboxyhemoglobin, improving systemic oxygen delivery and reversing the inhibitory effects of CO on mitochondria. We conclude that Ngb-H64Q-CCC or other CO scavengers demonstrate potential as antidotes that reverse the clinical and molecular effects of CO poisoning.

Compartment syndrome in the forearm related to carbon monoxide intoxication: case report

Introduction: Carbon monoxide (CO) poisoning is one of the most common forms of intoxication around the world. One of the complications associated with CO exposure is direct toxicity to the skeletal muscles. Though compartment syndrome induced by CO intoxication is rare, it is a well-known complication. In this study, we present a case of CO poisoning in a patient who developed compartment syndrome in his forearm. Case report: A 22-year-old man was found unconscious in a motel where a briquette had burned. He was later diagnosed with rhabdomyolysis associated with CO poison- ing. After he regained consciousness, he experienced difficulty in moving his left arm, with sensory impairment in the same arm. He was diagnosed with compartment syndrome, and an emergency fasciotomy was performed. One month later, electromyography was performed which revealed left median, ulnar, radial and musculocutaneous nerve palsy. Discussion: Compartment syndrome induced by CO intoxication is rare but is a well-known complication. Compartment syndrome is a limb-threatening and life- threatening condition. If untreated, the pressure in the muscle may rise, which can lead to tissue necrosis. Generally, nerve paralysis does not occur in CO poisoning. In our case, it occurred as median, ulnar, radial and musculocutaneous nerve palsy. Conclusion: Side effects of CO poisoning can be extant, especially for those who are unconscious since they cannot express pain, numbness, and motor weakness. It is important to not overlook compartment syndrome, to double-check whether there is swelling, change in skin color, or skin firmness in extremities, and to observe the patient closely.

Immediate and Delayed Neuropsychological Effects of Carbon Monoxide Poisoning: A Meta-analysis.

Carbon monoxide (CO) poisoning is the leading cause of accidental poisoning worldwide. This study undertook a meta-analysis to examine differences in neuropsychological functioning in patients with CO poisoning as compared to healthy controls, and examined the longer-term neuropsychological effects of CO poisoning. Studies performed between the years 1995 and 2016 were identified through a search of the electronic databases Medline and PsycInfo. Data from the papers identified were pooled to determine standard mean differences using a random-effects model. Ten studies were included in the analysis, with healthy controls performing significantly better than CO poisoned participants on the domains of divided attention, immediate memory, and processing speed. No statistically significant differences were found for sustained attention, recent memory, working memory, visuospatial/constructional ability, and expressive language. Performance by participants with CO poisoning for the domains of sustained attention, recent memory, visuospatial/constructional abilities, and working memory significantly improved over time after initial exposure, demonstrating recovery of these functions over time. No statistically significant differences were evident for divided attention or expressive language. This evidence indicates that healthy controls perform better than do individuals with CO poisoning on a range of neuropsychological domains; however, it also indicates that performance in some domains does improve over time. (JINS, 2018, 24, 405-415).

Predicting Cardiotoxic Effects of Carbon Monoxide Poisoning Using Speckle Tracking Echocardiography.

Carbon monoxide (CO) poisoning could cause significant cardiac injury. This study aimed to evaluate patients with CO poisoning by using speckle tracking echocardiography (STE), a potentially more sensitive technique, to identify left systolic ventricular dysfunction for the first time in the literature. Seventy-two patients who were exposed to CO poisoning were studied. Blood collection and echocardiography were performed at admission and after patients' discharge on days 10-15 (mean 12days). Global longitudinal strain (GLS) and global circumferential strain (GCS) were calculated using STE. In order to find the normal strain levels and to compare it to the patient with CO poisoning, 35 healthy subjects were included in the study. Left ventricular ejection fraction was analyzed according to Simpson's method. Patients were divided into two groups based on their LVEF values. LVEF<55%, Group 1 (n=24); LVEF≥55%, Group 2 (n=48). The reduction in Group 1 strain levels decreased in correlation with LVEF (p<0.001) while in Group 2, there were no significant changes in LVEF but strain levels were significantly reduced (p=0.091; p<0.001). Compared with the control group patients, admission GLS and GLC values of CO-poisoned patients were significantly low both in Group 1 and 2. On the contrary, no significant difference was observed when compared with follow-up GLS value. For prediction of CO cardiotoxicity, the cutoff value of GLS was ≥ -19.1 with a sensitivity of 70.3% and a specificity of 100% [(AUC) 0.840, 95% (CI) 0.735-0.916; p<0.001] in the ROC curve analyses. GLS was found as independent predictors of cardiotoxicity. Our study demonstrates the potential of using systolic strain values obtained using 2D-STE in determining cardiotoxicity due to CO poisoning. Speckle tracking echocardiography has the potential of demonstrating subtle LV systolic dysfunction even in CO poisoning patients with preserved EF.

The Effect of Carbon Monoxide Poisoning on Platelet Volume in Children

The Effect of Carbon Monoxide Poisoning on Platelet Volume in Children

Carbon Monoxide Poisoning: Pathogenesis, Management, and Future Directions of Therapy.

Carbon monoxide (CO) poisoning affects 50,000 people a year in the United States. The clinical presentation runs a spectrum, ranging from headache and dizziness to coma and death, with a mortality rate ranging from 1 to 3%. A significant number of patients who survive CO poisoning suffer from long-term neurological and affective sequelae. The neurologic deficits do not necessarily correlate with blood CO levels but likely result from the pleiotropic effects of CO on cellular mitochondrial respiration, cellular energy utilization, inflammation, and free radical generation, especially in the brain and heart. Long-term neurocognitive deficits occur in 15-40% of patients, whereas approximately one-third of moderate to severely poisoned patients exhibit cardiac dysfunction, including arrhythmia, left ventricular systolic dysfunction, and myocardial infarction. Imaging studies reveal cerebral white matter hyperintensities, with delayed posthypoxic leukoencephalopathy or diffuse brain atrophy. Management of these patients requires the identification of accompanying drug ingestions, especially in the setting of intentional poisoning, fire-related toxic gas exposures, and inhalational injuries. Conventional therapy is limited to normobaric and hyperbaric oxygen, with no available antidotal therapy. Although hyperbaric oxygen significantly reduces the permanent neurological and affective effects of CO poisoning, a portion of survivors still have substantial morbidity. There has been some early success in therapies targeting the downstream inflammatory and oxidative effects of CO poisoning. New methods to directly target the toxic effect of CO, such as CO scavenging agents, are currently under development.

Uncommon MRI and Echocardiographic Findings in a Patient of Carbon Monoxide Poisoning

Carbon Monoxide (CO) is a colorless and odorless gas which is nonirritating and is produced whenever there is incomplete combustion of any fossil fuel. There are diverse clinical effects of CO poisoning and they may be easily confused with other illnesses, such as nonspecific viral illness, benign headache, and various cardiovascular and neurologic conditions. Although initial neurologic manifestations may be subtle, but more profound exposure may produce altered mental status, confusion, syncope, seizure, acute stroke-like syndromes, and coma. Isolated seizures have been reported more often in pediatric patients. The cardiovascular effects of CO poisoning are manifested initially by tachycardia in response to hypoxia but more significant exposures may result in hypotension, arrhythmias, ischemia, infarction and even cardiac arrest. We present here an interesting case of one such patient who presented with features of severe myocardial depression and uncommon MRI findings secondary to carbon monoxide poisoning

A Case of Neuropsychological Sequelae of Carbon Monoxide Poisoning Treated with Hyperbaric Oxygen Therapy

Carbon Monoxide is one of the most common causes of inhalation poisoning worldwide and can result in significant morbidity due to persistent neuropathology and cognitive sequelae. The manifestation of carbon monoxide poisoning are non specific and severity of symptoms range from mild such as headache, confusion, lack of energy to severe, such as coma, respiratory depression, cardiac dysfunction and even death. Hyperbaric oxygen therapy has been used for decades in the treatment of acute and delayed effects of carbon monoxide poisoning. Hyperbaric Oxygen is the only treatment for acute CO poisoning where it competes with CarboxyHemoglobin preventing the resultant damage and in delayed neuropsychological sequelae. This case report is of a young lady from rural Haryana presented after 48 hours of CO Poisoning with acute confusion, partial retrograde and complete anterograde memory loss. Following 15 days of hyperbaric oxygen she showed near complete recovery and her Mini Mental Scale Examination (MMSE) score which was 12/30 on the first day went up to 29/30. This case demonstrates that HBO therapy is efficacious in recovery of delayed neuropsychiatric sequelae of Carbon Monoxide poisoning.

Catalytic activity of ultrathin Pt films on aligned carbon nanotube arrays

Uniform ultrathin Pt films were electrodeposited onto an aligned array of carbon nanotubes (CNTs) for high-area chemically stable methanol fuel cell anodes. Electrochemical treatment of the graphitic CNT surfaces by diazoniumbenzoic acid allowed for uniform Pt electroplating. The mass activity of the Pt thin film can reach 400 A/g at a scan rate of 20 mV/s and in a solution of 1 M CH 3OH/0.5 M H 2SO 4. A programmed pulse potential at 0 V was also seen to nearly eliminate the effects of carbon monoxide poisoning. The mass activity of Pt for methanol oxidation can be maintained at 300 A/g for more than 3000 s, which is 19 times of that under a constant potential of 0.7 V (vs. Ag/AgCl).

Late stent thrombosis secondary to carbon monoxide poisoning

Carbon monoxide poisoning has a variety of deleterious cardiac effects including arrhythmias, coronary spasm and myocardial infarction. The pro-thrombotic effect of carbon monoxide poisoning is one of the important postulated mechanisms of cardiac injury. There are multiple case reports of myocardial infarction secondary to carbon monoxide poisoning. However, there is no published case of carbon-monoxide-poisoning-induced stent thrombosis. We present a 50-year-old female with late stent thrombosis of a sirolimus-eluting stent secondary to acute carbon monoxide poisoning.

The effect of carbon monoxide poisoning on hemorheological parameters in rats and the alterations in these parameters in response to three kinds of treatments

This study aimed to investigate the short term effects of carbon monoxide (CO) poisoning and three kinds of poisoning treatments; namely room air, normobaric and hyperbaric oxygen on hemorheological parameters such as red blood cell (RBC) deformability, aggregation, blood and plasma viscosity. 43 Wistar rats were divided into 5 groups. Poisoning was induced by exposure to 4000 ppm CO (1 h). The poisoning protocol was followed by 3 types of treatments; room air, normobaric 100% oxygen and hyperbaric oxygen for 1 h. RBC deformability and aggregation were determined using an ektacytometer (LORCA) and a cone-plate rotational viscometer was used for the viscosity measurements. RBC deformability of CO poisoned rats were found to be elevated and the treatments applied, caused decrement of this parameter. A no significant increment tendency was found in erythrocyte aggregation after CO exposure. Although room air and hyperbaric oxygen treatments caused further significant elevations in the amplitude of aggregation, normobaric oxygen therapy induced decrement in this parameter towards control levels. No significant alterations were observed in viscosity values among the groups. The results of this study demonstrate normobaric oxygen therapy as a better choice of treatment after CO poisoning in hemorheological point of view.

1H MR spectroscopy of gray and white matter in carbon monoxide poisoning

Carbon monoxide (CO) intoxication leads to acute and chronic neurological deficits, but little is known about the specific noxious mechanisms. (1)H magnetic resonance spectroscopy (MRS) may allow insight into the pathophysiology of CO poisoning by monitoring neurochemical disturbances, yet only limited information is available to date on the use of this protocol in determining the neurological effects of CO poisoning. To further examine the short-term and long-term effects of CO on the central nervous system, we have studied seven patients with CO poisoning assessed by gray and white matter MRS, magnetic resonance imaging (MRI) and neuropsychological testing. Five patients suffered from acute high-dose CO intoxication and were in coma for 1-6 days. In these patients, MRI revealed hyperintensities of the white matter and globus pallidus and also showed increased choline (Cho) and decreased N-acetyl aspartate (NAA) ratios to creatine (Cr), predominantly in the white matter. Lactate peaks were detected in two patients during the early phase of high-dose CO poisoning. Two patients with chronic low-dose CO exposure and without loss of consciousness had normal MRI and MRS scans. On follow-up. five of our seven patients had long-lasting intellectual impairment, including one individual with low-dose CO exposure. The MRS results showed persisting biochemical alterations despite the MRI scan showing normalization of morphological changes. In conclusion, the MRS was normal in patients suffering from chronic low-dose CO exposure; in contrast, patients with high-dose exposure showed abnormal gray and white matter levels of NAA/Cr, Cho/Cr and lactate, as detected by (1)H MRS, suggesting disturbances of neuronal function, membrane metabolism and anaerobic energy metabolism, respectively. Early increases in Cho/Cr and decreases of NAA/Cr may be related to a poor long-term outcome, but confirmation by future studies is needed.

103: Acute Cardiac Effects of Carbon Monoxide Poisoning in Children

Carbon monoxide (CO) poisoning is associated with a high incidence of morbidity and mortality. Infants and children may have an increased susceptibility to CO toxicity because of their higher basal metabolic rate and consequent higher tissue oxygen demand. The clinical presentation is non-specific and may range from nausea and headache to profound central nervous system dysfunction, cardiac failure, arrythmia and death. However, CO-induced cardiotoxicity has been infrequently investigated in children and its cardiovascular effects are limited to isolated case reports. Our aim is to describe acute cardiac manifestations of CO poisoning in children.

The discovery and rediscovery of oxygen

The therapeutic use of oxygen was pioneered in the early 20 th century by the respiratory physiologist John Scott Haldane. His work followed Claude Bernard’s description of the toxic effects of carbon monoxide. Haldane, having also observed the effects of carbon monoxide poisoning, became aware of the therapeutic benefits of oxygen in this condition. He was also an advocate of oxygen as a therapeutic agent in other respiratory illness, and made efforts to define how the gas could best be administered. The history of identification of oxygen as a chemical element is convoluted. In the 17 th century, the controversial John Mayow suggested that only a portion of air was necessary for sustaining life. Mayow’s work was largely overlooked during his lifetime, and his insight was subsequently eclipsed by the phlogiston theory, an erroneous concept widely believed for nearly a century after his death. This theory was ultimately disproved by Joseph Priestley in 1774. Although the point of primacy is somewhat contentious, Priestley shares the distinction of discovering elemental oxygen with Antoine-Laurent Lavoisier, the French chemist, and Carl Wilhelm Scheele, the Swedish apothecary.

Effects of Carbon Monoxide Poisoning on Neutrophil Responses in Patients Treated with Hyperbaric Oxygen

Background Carbon monoxide (CO) poisoning can cause tissue injury. Neutrophil granulocytes have been proposed to contribute to the injury, which may be ameliorated by hyperbaric oxygen (HBO2) treatment. We sought to assess the relationship between acute CO poisoning and blood neutrophil count, plasma cytokine, and Cortisol responses, as well as the mechanism behind the observed beneficiary effects of HBO2 treatment. Methods Eight patients (age 26–82 years) with severe acute CO poisoning were enrolled, concomitant with eight healthy controls (age 27–42 years), in a prospective, controlled, clinical study. The patients were given three HBO2 treatments (2.8 atmospheres absolute, 100 minutes) within the first 24 hours. The controls were given identical simultaneous HBO2 treatments. Venous blood samples were taken before and after each treatment. Results At the start of the HBO2 treatment, patients displayed significantly higher blood neutrophil counts ( p &lt; .0001) and plasma Cortisol levels (p = .020) than controls, but the two groups had similar values for interleukin-8, granulocyte colony-stimulating factor (G-CSF), neutrophil H2O2 generation, and CD16 and CD18 surface expression. During the observation time, neutrophil H2O2 accumulation declined in patients and in controls ( p = .031), whereas the up-regulation of CD18 expression increased ( p = .002) in both groups. Moreover, G-CSF levels became significantly higher in patients than in controls ( p = .015). G-CSF levels also correlated significantly with neutrophil counts. Conclusion CO poisoning was associated with discrete changes of blood neutrophil counts, Cortisol, and G-CSF plasma concentrations. HBO2 treatment modulated neutrophil generation of H2O2 and surface expression of CD18. These changes may be part of the cascade of events leading to the sequelae of CO poisoning and their attenuation by HBO2.

Effects of Carbon Monoxide Poisoning on Neutrophil Responses in Patients Treated with Hyperbaric Oxygen

Effects of Carbon Monoxide Poisoning on Neutrophil Responses in Patients Treated with Hyperbaric Oxygen