جستجوی مقالات مرتبط با کلیدواژه "carbon monoxide poisoning" در نشریات گروه "پزشکی"

Carbon monoxide (CO) intoxication is one of the most important poisonings related to high morbidity and mortality rate. The main treatment of CO poisoning is oxygen therapy using normobaric (NBO) or hyperbaric oxygen (HBO). However, more pharmaceutical agents are needed to improve CO poisoning treatment, especially in severe cases. Recently, erythropoietin (EPO) has been examined in several studies, showing a significant reduction in cardiac and neural sequels of CO poisoning.In this article, the effect of EPO on cardio and neurotoxicity of CO poisoning were reviewed. For this purpose, EPO effect on CO poisoning was searched in papers published until 2020 using Pubmed, Scopus, and google scholar. Only English papers on three main databases have been reviewed. The review of several animal and clinical studies have been shown that EPO administration after CO poisoning could improve neurological function and reduce CO-neurotoxicity significantly. Although there is good evidence of EPO effects on CO-induced-neurological sequelae, further clinical studies are needed to establish its benefit on CO intoxication.

Carbon monoxide (CO) poisoning is the leading cause of poisoning-related deaths in theUnited States. In addition, myocardial infarction (MI) due to CO poisoning in a young, healthy adult is rare.On the other hand, smokeless tobacco, processed in various forms, is a controversial coronary heart disease(CHD) risk factor.

CASE REPORT: 

In this study, we describe a 29-year-old man who presented with acute chest pain followinga night of smoking tobacco and using smokeless tobacco in the presence of carbon monoxide poisoning.ST-segment elevation was observed on an electrocardiogram, and echocardiography revealed akinesia. Inaddition, cardiac markers were elevated. In this particular instance, thrombolytic therapy demonstratedsuccessful outcomes.

We believe the case and discussion could shed light on the emergency departmentmanagement of such individuals. We advise clinicians to consider the possibility of coronary heart diseasein carbon monoxide poisoning patients and to obtain a baseline electrocardiogram and cardiac markers.

Poisoning with carbon monoxide occurs occasionally worldwide, and the gold diagnostic standard is to measure carboxyhemoglobin level in the blood. This study investigated the correlation between carboxyhemoglobin and the end-tidal carbon dioxide levels in 50 patients with carbon monoxide poisoning.

We recruited 50 volunteer patients who had been admitted to the Emergency Services of Istanbul Medipol University Hospital between January 2017 and January 2018. They had been diagnosed with carbon monoxide poisoning unrelated to fire accidents. The arterial and venous blood gases, and other blood and clinical parameters were also measured. The patients’ end-tidal carbon dioxide levels were measured from the nose and mouth air, using a Capnostream 20p bedside monitor. Pearson’s correlation analyses were performed and the results were compared with the end-tidal carbon dioxide, carboxyhemoglobin and oxygen saturation in the arterial and venous blood samples.

The Mean±SD age was 33.98±10.89 years. The Mean±SD arterial and venous carboxyhemoglobin values were 18.05±7.10 and 12.11±9.67, respectively. There were no statistically significant differences between the oxygen saturation, and the arterial and venous blood levels of carboxyhemoglobin (P=0.870, P=0.950), respectively. Also, no statistically significant correlations were found between the end-tidal carbon dioxide, and the arterial and venous carboxyhemoglobin levels (P=0.529, P=0.601), respectively.

The results from the blood analyses demonstrated that there was no statistically significant difference between the end-tidal carbon dioxide and the carboxyhemoglobin levels in these patients who had been earlier diagnosed with carbon monoxide poisoning, unrelated to fire accidents.

Carbon monoxide (CO) poisoning is a widespread cause of morbidity and mortality, with delayed neurological Sequelae  (DNS) among the most severe consequences of this silent killer. To study the relationship between neutrophil-lymphocyte ratio (NLR), ischemia-modified albumin (IMA), and severity of acute CO poisoning as well as their role in predicting delayed neurological manifestations.Patients and Sixty acutely CO-intoxicated patients were admitted to Alexandria Poison Center, Egypt. NLR and IMA were assessed. Six months after discharge, all patients were subjected to neuropsychometric testing using Mini-Mental Status Examination (MMSE). Brain magnetic resonance imaging (MRI) was conducted on cognitively impaired patients. NLR was abnormally high in most patients and the mean serum level of IMA was significantly elevated in acutely CO-intoxicated patients compared to the control group (P<0.001). NLR and IMA were significantly related to neurological manifestations and other laboratory parameters. Patients were subdivided into DNS group (n = 16) and non-DNS group (n = 44), according to MMSE and brain MRI done after six months, with significant elevation of NLR and IMA in DNS group (p<0.001). The accuracy of DNS prediction parameters was measured using the area under the receiver operating characteristics curve. Excellent accuracy was detected for IMA and NLR. The studied markers of NLR and IMA assessed on admission could be employed as useful biomarkers for correlating with acute CO poisoning severity and predicting the outcome including the possibility of development of DNS.

Carbon monoxide (CO) poisoning is a prevalent lethal condition. The clinical feature of this type of poisoning varies from headache and nausea to more severe conditions. After recovery from the acute intoxication, neurological or behavioral problems may emerge. In 3%-40% of cases, delayed neuropsychiatric syndrome (DNS) in post CO poisoning, generally develops within few weeks after a preliminary remission from acute poisoning.

We report a patient with relatively suitable premorbid. He was admitted to the hospital with fire burning, co poisoning and discharged home with good general conditions and mental status by receiving normal baric oxygen 100%. later in post-operative management of skin graft he developed a fulminant neurological deficit by impaired memory and concentration, loosening of association, disorientation to place, time and person, agitation, aggression, mood labiality, urinary incontinency and encopresis, slow psychomotor retardation, false and approximate answers to questions, auditory and visual hallucination, staring and inappropriate laughing. As the patient was not responsive to neurological treatment, he was referred to psychiatric service. DNS in this patient resolved gradually during a short period of psychopharmacotherapy and supportive psychotherapy.

CO poisoning may lead to neuropsychiatric sequel and neuroimaging changes which could be reversible.

Cardiotoxicity is one of the major consequences in carbon monoxide poisoning. Following our previous work, in this study we aimed to define the myocardium changes induced by carbon monoxide (CO) intoxication and evaluate erythropoietin (EPO) effect on CO cardiotoxicity in rat.
Severe carbon monoxide toxicity induced by 3000 ppm CO in Wistar rat. EPO was administrated (5000 IU/Kg, intraperitoneal injection) at the end of CO exposure and then the animals were re-oxygenated with the ambient air. Subsequently heart was removed and assessed by histopathology and electron microscopy examinations.
3000 ppm CO induced significant myocardium injury; multiple foci of necrosis and lymphocyte infiltration compare with the control (P˂0.05). Electron microscopy examination showed myofibril lysis and mitochondrial swelling in myocardium due to 3000 ppm CO poisoning. However EPO administration after CO exposure resulted in significant reduction in cardiomyocytes injury (P˂0.05).
Our results represented protective effect of EPO on cardiac injury induced by CO intoxication in rat.

Intoxication due to carbon monoxide (CO) is one of the most common types of poisoning. Cardiac effects of carboxyhemoglobin (COHb) range from simple arrhythmias to myocardial infarction..
The current study aimed to investigate the relationship between blood carboxyhemoglobin and high-sensitivity cardiac troponin T (hs-cTnT) level with a highly sensitive assay in patients with acute carbon monoxide poisoning..
Patients and This retrospective study was conducted on 141 (54 males and 87 females) patients, with acute CO intoxication, admitted to the Sevket Yilmaz research and education hospital emergency unit during a one-year period (January 2012 - January 2013). The patients were divided into three groups based on COHb levels: Group I, mild COHb level 25%. COHb, hs-cTnT (Stat), creatine kinase (CK) and creatine kinase-myocardial band (CK-MB) levels were measured on admission..
The mean age of the patients was 38 ± 16 years. COHb levels ranged from 8 to 35. hs-cTnT levels on inclusion in this study were slightly different between the groups (P = 0.05). COHb levels with hs-cTnT values were weakly correlated (r = 0.173, P = 0.041); on the other hand, CK-MB levels were not correlated with COHb (r = 0.013, P = 0.883)..
In patients without clear signs of myocardial infarction, even mild CO poisoning was associated with quantifiable circulating levels of hs-cTnT when TnT was measured using a highly sensitive assay in the current study patients. Plasma levels of the hs-TnT and CK-MB assays were not correlated with the COHb levels in the current study patients..

Knowing the pattern of carbon monoxide (CO) poisoning in each region is vital for enhanced health planning. This study was designed to evaluate the epidemiologic pattern of unintentional acute CO poisoning in major cities of Fars province, southwest of Iran.
This one-year cross-sectional study was carried out on unintentional CO poisoning incidents in Fars province, Iran, during the year 2011. The target population was people living in 7 major cities under supervision of Shiraz University of Medical Sciences including Shiraz, Eghlid, Neyriz, Khorambid, Marvdasht, Darab and Bavanat.
During 2011, 111 CO poisoning events occurred in the catchment area. These events involved 420 individuals (50.2% men) who were present during the poisoning event, of which 281 individuals with mean age of 27.8 ± 14.8 years were poisoned (46.5% men). The majority of CO poisoning events (77.3%) occurred in colder months of the year. Most events happened in urban areas (61.3%). The most common source of CO was water heater (27.5%) closely followed by gas stove (24.8%). The majority of poisoned patients were asleep during the event (150/281: 53.3%). The main causes of CO generation were inbound gas return (62.2%) and inappropriate ventilation (28.8%). The fatality rate of CO poisoning was significantly higher in men compared to women both in involved individuals and poisoned patients (P = 0.035, Generally, the incidence and fatality rate of CO poisoning in the current study were comparable to those of the world statistics, but higher than in developed counties. Attention and emphasis on the safety of gas heaters, stoves, and other gas-powered appliances in residential places should be enforced.

Carbon monoxide (CO) poisoning has remained a common, serious and often unrecognized event and constitutes a public health problem in Morocco. The objective of this study is to describe the epidemiological and clinical profile and risk factors of CO poisoning in the region of Fez-Boulemane, Morocco. This is a retrospective study on CO poisoning cases occurred in the region of Fez-Boulemane between January 2009 and December 2012. Data were retrieved from medical records of patients who were admitted to 7 referral hospitals in the study catchment area. The patient's clinical status was classified according to the Poisoning Severity Score. By comparing critical (grade 3 or 4) and non-critical (grade 1 or 2) cases, a univariate analysis was performed to identify the factors associated with life-threatening consequences. During the study period, 2332 cases were included. Most patients were women (68%). The mean (SD) age of patients was 26.4 (16.1) years. Most cases occurred during winter (45.1%). The source of poisoning was water heaters in majority of cases (53%). The most common manifestations were headache in 86%, nausea in 79%, dizziness in 76%, vomiting in 63% and dyspnea in 63% of cases. The majority of patients had grade 2 or grade 1 poisoning severity. Univariate analysis demonstrated that gender (P = 0.03) and the location of event (P = 0.005) had significant impacts on the prognosis while age did not have any influence on the severity of poisoning (P = 0.15). The impact of season of event on the prognosis approached the level of significance but its significance was questionable (P = 0.09). This study showed that CO poisoning is common but probably underestimated in the region. Strengthening the role of the morocco poison control center in the region would be the most effective preventive measure to decrease morbidity and mortality secondary to CO poisoning.

The aim of this study was to define the electrocardiogram (ECG) changes following the moderate to severe CO intoxication in rats, and also evaluating the effect of erythropoietin (EPO) on observed cardiac disturbances. The growing literature on erythropoietin effect on cardiac ischemia led us to question its effect on cardiotoxicity due to the carbon monoxide poisoning. Wistar rats were exposed to three different concentrations of CO (250 PPM, 1000 PPM or 3000 PPM). EPO was administrated (5000 IU/Kg, intraperitoneal injection) at the end of CO exposure and then the animals were re-oxygenated with ambient air. Subsequently ECG recording, heart rate and carboxyhemoglobin values were evaluated. ECG changes following the CO intoxication included ST segment elevation and depression, T wave inversion and first-degree AV block. Ischemic ECG changes reduced significantly in EPO-treated animals. In the present study, for the first time, EPO was investigated for the management of cardiac complications due to the CO poisoning. Our results showed that EPO could inhibit ischemic changes of ECG after the CO poisoning.