Brugada Electrocardiographic Pattern in Carbon Monoxide Poisoning

Purpose: This study was conducted to describe the characteristics of patients with carbon monoxide (CO) poisoning. Methods: We retrospectively surveyed data from the Emergency Department based Injury In-depth Surveillance of 20 hospitals (2011-2014). We included patients whose mechanism of injury was acute CO poisoning caused by inhalation of gases from charcoal or briquettes. We surveyed the annual frequency, gender, age, result of emergency treatment, rate of intensive care unit (ICU) admission, result of admission, association with alcohol, and place of accident. We also surveyed the cause and experience of past suicide attempts by intentional poisoning. Results: A total of 3,405 patients were included (2,015 (59.2%) and 1,390 (40.8%) males and females, respectively) with a mean age of $39.83{pm}18.51$ year old. The results revealed that the annual frequency of CO poisoning had increased and the frequency of unintentional CO poisoning was higher than that of intentional CO poisoning in January, February and December. The mean age of intentional CO poisoning was younger than that of unintentional CO poisoning ($38.41{pm}13.03$ vs $40.95{pm}21.83$) (p<0.001). The rates of discharge against medical advice (DAMA), ICU care and alcohol association for intentional CO poisoning were higher than for unintentional CO poisoning (36.4% vs 14.0%, 17.8% vs 4.7%, 45.2% vs 5.6%) (p<0.001). The most common place of CO poisoning was in one's residence. Conclusion: The annual frequency of total CO poisoning has increased, and unintentional CO poisoning showed seasonal variation. DAMA, ICU care, and alcohol association of intentional CO poisoning were higher than those of unintentional CO poisoning.

To examine the serum level of myocardial injury markers in patients with carbon monoxide (CO) poisoning, the correlation between these markers and the severity of the disease, and the therapeutic effects of L-carnitine administration. 69 patients, chosen from 309 cases of acute carbon monoxide poisoning (ACOP) for abnormally high level of serum myocardial injury markers (myoglobin, Mb; MB isoenzyme of creatine kinase, CK-MB; cardiac troponin-I, cTnI) at the time of admission, were randomly divided into control group (n = 34) and observation group (n = 35). The patients in control group were given Xingnaojing (20 ml/d i.v. drip), and the observation group Xingnaojing (20 ml/d)+L-carnitine (2 g/d i.v. drip), in addition to the conventional oxygen supply and symptom-focused therapy. The plasma concentration of carboxyhemoglobin (HbCO, as index for CO poisoning severity), Mb, CK-MB, and cTnI in these patients were further examined 24 hours, 72 hours and 1 week after the treatment, for difference between the two groups, and the correlation between the serum level of HbCO and the myocardial injury markers. At the time of admission, the incidence of abnormal findings in myocardial injury markers were 2.5% (5/204), 46.8% (36/77) and 100.0% (28/28) in patients with mild (HbCO: 10% ~ 19%), moderate (20% ~ 39%) and severe (≥40%) CO poisoning, respectively. The incidence of abnormal findings in injury markers was significantly correlated to the HbCO concentration (x(2)=170.3549, P < 0.0001). Before the treatment, no significant difference was found in any of the indexes [HbCO: (31.1 ± 17.6)%, (32.3 ± 16.9)%, Mb (μg/L): 154.2 ± 51.8, 165.4 ± 48.6, CK-MB (μg/L): 8.7 ± 3.3, 9.6 ± 3.8), and cTnI (μg/L): 2.7 ± 1.2, 2.8 ± 1.5, all P > 0.05] between the control and observation group. However, it was found in: Mb (24 hours: 74.0 ± 36.5 vs. 97.1 ± 35.8, 72 hours: 40.1 ± 6.8 vs. 69.0 ± 11.2), cTnI (24 hours: 1.9 ± 0.5 vs. 2.3 ± 0.7, 72 hours: 1.2 ± 0.3 vs. 1.8 ± 0.4) both 24 hours and 72 hours after the treatment, and CK-MB, 24 hours after treatment (10.6 ± 4.1 vs. 13.0 ± 3.9) with the values in observation group significantly lower (P < 0.05 or P < 0.01); 1 week after the treatment, the concentration of all the injury markers returned to the normal levels with no significant difference between the two groups. Meanwhile, no significant difference was found between the two groups in HbCO concentration throughout the due-course of the therapy. The incidence of abnormal findings in serum myocardial injury markers was positively correlated with HbCO concentration after CO poisoning. L-carnitine may protect the myocardium and striated muscles against injury in patients with CO poisoning.

Risk of Venous Thromboembolism After Carbon Monoxide Poisoning: A Nationwide Population-Based Study

Acute carbon monoxide (CO) poisoning is the most common cause of poisoning and poisoning-related death in the United States. It manifests as broad spectrum of symptoms ranging from mild headache, nausea, and fatigue to dizziness, syncope, coma, seizures resulting in cardiovascular collapse, respiratory failure, and death. Cardiovascular complications of CO poisoning has been well reported and include myocardial stunning, left ventricular dysfunction, pulmonary edema, and arrhythmias. Acute myocardial ischemia has also been reported from increased thrombogenicity due to CO poisoning. Myocardial toxicity from CO exposure is associated with increased short-term and long-term mortality. Carboxyhemoglobin (COHb) levels do not correlate well with the clinical severity of CO poisoning. Supplemental oxygen remains the cornerstone of therapy for CO poisoning. Hyperbaric oxygen therapy increases CO elimination and has been used with wide variability in patients with evidence of neurological and myocardial injury from CO poisoning, but its benefit in limiting or reversing cardiac injury is unknown. We present a comprehensive review of literature on cardiovascular manifestations of CO poisoning and propose a diagnostic algorithm for managing patients with CO poisoning.

Utilizing Syndromic Surveillance for Hurricane Irma-Related CO Poisonings in Florida

Carbon monoxide (CO) poisoning is a leading cause of morbidity and mortality during natural disasters. On January 26-27, 2009, a severe ice storm occurred in Kentucky, causing widespread, extended power outages and disrupting transportation and communications. After the storm, CO poisonings were reported throughout the state. The objectives of this investigation were to determine the extent of the problem, identify sources of CO poisoning, characterize cases, make recommendations to reduce morbidity and mortality, and develop prevention strategies. We obtained data from the Kentucky Regional Poison Center (KRPC), hyperbaric oxygen treatment (HBOT) facilities, and coroners. Additionally, the Kentucky Department for Public Health provided statewide emergency department (ED) and hospitalization data. During the two weeks after the storm, KRPC identified 144 cases of CO poisoning; exposure sources included kerosene heaters, generators, and propane heaters. Hospitals reported 202 ED visits and 26 admissions. Twenty-eight people received HBOT. Ten deaths were attributed to CO poisoning, eight of which were related to inappropriate generator location. Higher rates of CO poisoning were reported in areas with the most ice accumulation. Although CO poisonings are preventable, they continue to occur in postdisaster situations. Recommendations include encouraging use of CO alarms, exploring use of engineering controls on generators to decrease CO exposure, providing specific information regarding safe use and placement of CO-producing devices, and using multiple communication methods to reach people without electricity.

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.

Muscle weakness has been repeatedly reported in patients with carbon monoxide (CO) intoxication. In animal models, CO intoxication has been linked with mitochondrial electron transport dysfunction. The objectives of the present study were to use Tc-99m sestamibi thigh single-photon emission computed tomography/computed tomography (SPECT/CT) to evaluate the mitochondrial status in patients with CO intoxication, correlate this with clinical parameters, and compare with age-matched controls. A total of 25 patients with delayed sequelae after CO intoxication (range: 1-60 months) and 17 sex- and age-matched healthy volunteers underwent Tc-99m sestamibi thigh SPECT/CT. Cognitive evaluation and muscle power according to medical research council (MRC) grading were collected. Both visual scoring from planar images and automatic volumetric analysis were used to rate the Tc-99m sestamibi uptake level. The visual scores showed that 14 patients (56.0%) were scored as moderate-to-severe decrement. Volumetric analysis showed that a significant Tc99m-sestamibi uptake decrement was found in the CO intoxication group as compared with the controls, and 16 patients (64.0%) had uptakes below 1 standard deviation of the control group. In the CO group, the muscle power but not the cognitive evaluation correlated with Tc-99m sestamibi uptake in muscles. The decrement of muscle Tc99m-sestamibi uptake was related to mitochondria swelling, increased mitochondrial numbers, and type II muscle atrophy in 1 patient. In this study, we demonstrated that patients with CO intoxication sustained defective mitochondrial metabolism in skeletal muscles as revealed by a decrement in Tc-99m sestamibi uptake either by visual or semiquantification of thigh SPECT/CT. Tc-99m sestamibi scanning provided noninvasive measurement of mitochondrial injury in muscles after CO intoxication and the correlation with clinical parameters was good.

There is no effective drug for the therapy of acute carbon monoxide (CO) poisoning. The purpose of the present study was to investigate the potential preventive and therapeutic effects of hemin on an animal model of acute CO poisoning and to provide a potential therapeutic candidate drug. A total of 80 Kunming mice were randomly divided into four groups, namely the air control, acute CO poisoning, hemin-treatment + CO and hemin-pretreatment + CO groups (n=20 each). Furthermore, the mortality rate of mice, blood carboxyhaemoglobin (HbCO) concentration and serum malondialdehyde (MDA) concentration were measured, and pathological changes of the hippocampal area were determined using histochemical staining. The mice with acute CO poisoning had a 50% mortality rate at 1 h, with an increase in blood HbCO, serum MDA levels and pathological impairments of the hippocampus. Furthermore, the mortality rate, blood HbCO and serum MDA levels of mice with pretreatment and treatment of hemin were decreased. Additionally, the pathological changes of the hippocampal area were improved in the hemin-treatment and hemin-pretreatment groups compared with the mice treated with CO. These results suggest that hemin is a novel effective chemical for the prevention and treatment of acute CO poisoning in mice. Therefore, the present study provides a novel method and experimental basis for the application of hemin in treating patients with acute CO poisoning.

White matter (WM) injury in carbon monoxide (CO) intoxication is thought to be related to delayed cognitive sequelae. To determine if microstructural changes in WM are responsible for the delayed onset of cognitive symptoms, we performed diffusion tensor imaging (DTI) in patients with CO intoxication. DTI was performed in 14 patients with delayed sequelae after CO intoxication and in 16 sex- and age-matched healthy volunteers. The fractional anisotropy (FA) and apparent diffusion coefficient (ADC) of several WM regions were measured. We also determined the correlation between FA of the selected WM and neuropsychological rating scores for the CO intoxication group. FA of patients with CO intoxication decreased in the corpus callosum, orbitofrontal WM, high frontal WM, parietal WM, and temporal lobes in comparison with the corresponding regions of healthy controls. FA of the WM in the occipital lobe and internal capsule of patients was not significantly different from that in controls. ADCs of all measured WM increased significantly in patients exposed to CO. High correlations were found between the FA of all selected WM and the Mini-Mental State Examination score (gamma = 0.631, P = .016) and the digit span backward task (gamma = 0.759, P = .001). CO intoxication may cause FA decline in associated cortical areas. This observation indicates microstructural WM pathology in CO intoxication, which is related to delayed cognitive encephalopathy.

Cerebral oedema is a major pathological change of acute carbon monoxide (CO) poisoning, the pathogenesis of which is still unclear. In the aquaporin (AQP) water channel family, AQP1 and AQP4 play critical roles in the progress of cerebral oedema of various neuropathological events. However, their functions in CO poisoning have not been demonstrated. In this study, we investigated the expressions of AQPs and associated mechanisms of brain injury in an acute CO poisoning rat model. Compared with the control injected intraperitoneally with equal volume of air, the dry weight/wet weight (DW/WW) ratio of brain water content, levels of AQP1, AQP4, phosph-p38 mitogen-activated protein kinase (p-p38 MAPK) and astrocyte marker, glial fibrillary acidic protein (GFAP) in the frontal cortex and hippocampal CA1 of acute CO poisoning group significantly increased at 6, 12, 24hours after CO injection. Intracerebroventricular injection with a p38 MAPK inhibitor, SB203580 (200µmol/L/kg/d), before CO injection reduced water content in the brain tissues and significantly decreased levels of AQP1, AQP4, p-p38 MAPK and GFAP. Therefore, our study showed that the overexpressions of AQP1 and AQP4 were involved in the development of CO poisoning-induced cerebral oedema, which could be attenuated by inhibition of p-p38 MAPK signalling. Manipulation of AQPs and p38 MAPK may be a new therapeutic strategy for acute CO poisoning.

More than one-third of patients with moderate to severe acute carbon monoxide (CO) poisoning had myocardial injury. However, the ratio of acute CO patients necessitating percutaneous coronary intervention (PCI) and coronary artery bypass grafting (CABG) remains unknown. This study aimed to examine the prevalence of myocardial injury requiring PCI or CABG in patients with CO poisoning. This was a nationwide retrospective cohort study, using the Japanese Diagnosis Procedure Combination inpatient database focusing on the period between 2010 and 2017. We extracted data on patients diagnosed with CO poisoning and determined the prevalence of cases presenting with myocardial injury requiring PCI or CABG. We identified 9091 eligible patients. Within this patient pool, eight patients underwent PCI within 2 days of admission. No patients required CABG. The prevalence of subsequent PCI was 0.09% (8/9091). The patients who required PCI had a significantly higher median age than those who did not (75 vs. 52 years of age, respectively). Patients requiring PCI were older and were more likely to have underlying comorbidities such as hypertension and diabetes mellitus. The present study reported a low prevalence of myocardial injury requiring PCI in acute CO poisoning patients. Although myocardial injury due to coronary artery occlusion would be a very rare presentation in the setting of acute CO poisoning, coronary occlusion should be taken into consideration for elderly patients and/or patients who have coronary risk factors.

Carbon monoxide (CO) poisoning is the leading cause of death from accidental poisoning worldwide. It is associated with significant mortality and morbidity. The mere notion of exposure to risk should lead to the diagnosis of CO poisoning in an emergency situation. Neurological (coma and delayed neuropsychological sequelae) and cardiac (ischemic changes with normal coronary arteries) clinical scenarios are explained by complex mechanisms: carboxyhemoglobin formation, cytochrome oxidase inhibition, oxidative stress, as well as ischemia-reperfusion phenomenon. Delayed neurological sequelae (DNS) or delayed encephalopathy is characterized by a neurological clinical picture that arises after acute CO intoxication and after a period of apparent recovery. The onset of DNS is unpredictable. The true prevalence of DNS is difficult to determine; the estimates range from 1% to 47% of patients after CO poisoning. The exact incidence rate is also unclear. Studies using rigorous methodologies, including neuropsychological testing, report the frequency to be as high as 67%. CO poisoning causes severe neurocognitive after-effects that are rarely studied in the literature. Here, we describe the case of a patient aged 18 years old with no known comorbidities, a victim of accidental CO poisoning, who initially presented with behavioral disorders. The evolution was marked by the occurrence of memory and attention disorders a few weeks later. Neuropsychological assessment revealed a dysfunction of several processes (executive, attentional, and memory). Brain MRI revealed restrictive bilateral occipital, frontal, and temporal lesions of hypoxic origin. The patient underwent three sessions of hyperbaric oxygen therapy and received symptomatic drug treatment and neurocognitive rehabilitation, with a more or less favorable evolution of her disorders.

Carbon monoxide (CO) poisoning is one of the leading causes of toxicity-related mortality and morbidity worldwide, primarily manifested by acute and delayed central nervous system (CNS) injuries and other organ damages. However, its definite pathogenesis is poorly understood. The aim of this study was to explore the pathogenesis of the ultrastructural and functional impairment of mitochondria and the protection of sulphoraphane (SFP) at different dosages on hippocampus neurons in rats after exposure to CO. We found that CO poisoning could induce advanced cognitive dysfunction, while the mitochondrial ultrastructure of neurons in rats of the CO poisoning group was seriously damaged and mitochondrial membrane potential (ΔΨm) was accordingly reduced by transmission electron microscopy (TEM) and JC-1 fluorescent probe assay. CO poisoning could also increase the expressions of both nuclear factor erythroid 2-related factor 2 (Nrf-2) and thioredoxin-1 (Trx-1) proteins and their mRNA in brain tissue with immunohistochemistry and quantitative PCR (qPCR) techniques. Early administration of either middle-dose or high-dose SFP could efficiently improve mitochondrial structure and function and enhance the antioxidative stress ability, thus exerting a positive effect against brain damage induced by acute CO poisoning.

Parkinsonism is a common neurological sequela of carbon monoxide (CO) poisoning, but its pathophysiological mechanism has yet to be clarified. To describe a married couple who were both affected by CO poisoning, but only 1 of whom developed CO-induced parkinsonism, and to discuss the possible underlying pathophysiological mechanism of CO-induced parkinsonism by comparing the neuroimaging findings of these patients. Case report from a clinical neurology department. A married couple experienced CO poisoning simultaneously. One month later, only the husband gradually developed delayed sequelae, including parkinsonism and intellectual impairment. On detailed neurological examination, the husband showed mild but definite rigidity and bradykinesia, while no parkinsonian signs were observed in the wife. Neuropsychological examination revealed impaired memory and attention in both patients, but they were more severe in the husband than in the wife. Magnetic resonance imaging scans of the patients' brains disclosed diffuse high-intensity white matter signals in both patients and bilateral pallidal necrosis in the wife. Dopamine transporter imaging showed that the degree of dopamine neuronal loss was comparable between these patients. Magnetic resonance spectroscopy revealed more severe white matter damage in the husband than in the wife. Thirteen months later, neurological and neuropsychological examinations showed complete recovery from parkinsonism as well as intellectual impairment. Follow-up magnetic resonance spectroscopy also suggested remarkable improvements in white matter damage. These results support the role of white matter damage in producing parkinsonism after CO poisoning and highlight the possible usefulness of magnetic resonance spectroscopy in predicting delayed sequelae in patients after CO poisoning. Arch Neurol. 2000;57:1214-1218