The Evaluation of Myocardial Damage in 83 Young Adults with Carbon Monoxide Poisoning in the East Anatolia Region in Turkey

2006 ◽  
Vol 25 (8) ◽  
pp. 439-446 ◽  
Author(s):  
Sahin Aslan ◽  
Mustafa Uzkeser ◽  
Bedri Seven ◽  
Fuat Gundogdu ◽  
Hamit Acemoglu ◽  
...  

Carbon monoxide (CO) poisoning is the leading cause of death from intoxication. In CO poisoning, it is important to know if there are any symptoms regarding myocardial damage, which are usually unobserved as a result of hypoxia. This study was planned to assess myocardial damage in young healthy patients with CO poisoning. Eighty-three young healthy cases who had been exposed to CO were included in this study. The demographic and clinical characteristics, the origin of CO gas and smoking habits of the patients were recorded. The evaluation of ECG, peripheral ABG, complete blood count and serial cardiac biomarkers (creatine kinase, creatine kinasemyocardial band and troponin I) measurements were performed in all cases. Additionally, echocardiogram (ECHO) and myocardial perfusion single-photon emission computed tomography (SPECT) were performed at the appropriate times in all cases. The mean age of the patients was 27.39 /10.9 years. The main complaint of the patients was loss of consciousness with a 62.7% rate. The average carboxyhaemoglobin level of the patients was 34.49 /15.9%. Sinus tachycardia was present in 26.5% of patients. Diagnostic ischaemic ECG changes were present in 14.4% of patients. In myocardial SPECT, myocardial ischaemic damage was observed in 9 cases, in 6 of whom ECHO findings were also confirmed. Myocar-dial damage due to CO poisoning should not be ignored. If patients are at risk in terms of myocardial damage, further studies, such as ECHO and scintigraphy are needed to determine myocardial damage resulting from CO poisoning. However, in the young adults of the risk group, if the baseline ECG and serial cardiac biomarkers are normal, further studies such as ECHO and scintigraphy, considering the length of exposure and the severity of poisoning, may not be necessary for the evaluation of myocardial damage due to CO poisoning.

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Hitoshi Koga ◽  
Hideki Tashiro ◽  
Kouta Mukasa ◽  
Tomohiro Inoue ◽  
Aya Okamoto ◽  
...  

Abstract Background Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is unclear, however, whether the indicators of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relationship between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning. Methods Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. Results The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P = 0.0072, R2 = 0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2358) and the corrected QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were corrected QT dispersion (P = 0.0042), and troponin I level (P = 0.0021). Conclusions Patients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.


2021 ◽  
pp. 096032712110434
Author(s):  
Yusuf K Tekin ◽  
Gülaçan Tekin ◽  
Naim Nur ◽  
İlhan Korkmaz ◽  
Sefa Yurtbay

Introduction The present study was undertaken to investigate the prognostic value of the frontal QRS-T angle associated with adverse cardiac outcomes in patients with carbon monoxide (CO) poisoning in early stages in the emergency department. Materials and methods The data of 212 patients with CO poisoning who were admitted to the ED between January 2010 and May 2020 were retrospectively analyzed. The frontal QRS-T angle was obtained from the automatic reports of the EKG device. Results Compared to patients without myocardial damage, among patients with myocardial damage, statistically high creatinine, creatine kinase MB, cardiac troponin I, and frontal QRS-T angle values were found ( p < 0.001 for all parameters), while the saturation of arterial blood pH and arterial oxygen values were found to be lower ( p = 0.002 and p < 0.001, respectively). The frontal QRS-T angle values were correlated with creatine kinase, creatine kinase-MB, cardiac troponin I, and oxygen saturation (SpO2) in arterial blood (r = 0. 232, p = 0.001; r = 0. 253, p = < 0.001; r = 0. 389, p = < 0.001; r = −0. 198, p = 0.004, respectively). The optimum cut-off value of the frontal QRS-T angle was found to be 44.5 (area under the curve: 0.901, 95% confidence interval: 0.814–0.988, sensitivity: 87%, specificity: 84%). Conclusions The frontal QRS-T angle, a simple and inexpensive parameter that can be easily obtained from 12-lead surface electrocardiography, can be used as an early indicator in the detection of myocardial damage in patients with CO poisoning.


2017 ◽  
Vol 37 (3) ◽  
pp. 240-246 ◽  
Author(s):  
YS Cha ◽  
H Kim ◽  
HH Do ◽  
HI Kim ◽  
OH Kim ◽  
...  

Delayed onset of neuropsychiatric symptoms after apparent recovery from acute carbon monoxide (CO) poisoning has been described as delayed neuropsychiatric sequelae (DNS). To date, there have been no studies on the utility of serum neuron-specific enolase (NSE), a marker of neuronal cell damage, as a predictive marker of DNS in acute CO poisoning. This retrospective observational study was performed on adult patients with acute CO poisoning consecutively treated over a 9-month period. Serum NSE was measured after emergency department arrival, and patients were divided into two groups. The DNS group comprised patients with delayed sequelae, while the non-DNS group included patients with none of these sequelae. A total of 98 patients with acute CO poisoning were enrolled in this study. DNS developed in eight patients. The median NSE value was significantly higher in the DNS group than in the non-DNS group. There was a statistical difference between the non-DNS group and the DNS group in terms of CO exposure time, Glasgow Coma Scale (GCS), loss of consciousness, creatinine kinase, and troponin I. GCS and NSE were the early predictors of development of DNS. The area under the curve according to the receiver operating characteristic curves of GCS, serum NSE, and GCS combined with serum NSE were 0.922, 0.836, and 0.969, respectively. In conclusion, initial GCS and NSE served as early predictors of development of DNS. Also, NSE might be a useful additional parameter that could improve the prediction accuracy of initial GCS.


2020 ◽  
Author(s):  
Hitoshi Koga ◽  
Hideki Tashiro ◽  
Kouta Mukasa ◽  
Tomohiro Inoue ◽  
Aya Okamoto ◽  
...  

Abstract Background: Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is not clear, however, whether the indices of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relation between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning.Results: Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P=0.0072, R2=0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P<0.001, R2=0.2358) and the corrected QT dispersion and carboxyhemoglobin (P<0.001, R2=0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were hyperbaric oxygen therapy (P=0.0182), corrected QT dispersion (P=0.0062), and troponin I level (P=0.0002).Conclusions: Patients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.


2020 ◽  
Author(s):  
Hitoshi Koga ◽  
Hideki Tashiro ◽  
Kouta Mukasa ◽  
Tomohiro Inoue ◽  
Aya Okamoto ◽  
...  

Abstract Background Carbon monoxide causes electrical, functional, and morphological changes in the heart. It is not clear, however, whether the indices of myocardial damage can predict the patient’s prognosis after carbon monoxide poisoning. This retrospective study aimed to investigate the relation between the carboxyhemoglobin level and electrocardiographic (ECG) changes and whether the ECG changes and troponin I levels are related to the patient’s prognosis after carbon monoxide poisoning. Results Carboxyhemoglobin, troponin I, and ECG parameters were measured in 70 patients with carbon monoxide poisoning. The QT and RR intervals were measured for each ECG lead in all patients, and the corrected QT interval and corrected QT dispersion were calculated. The correlation between the maximum corrected QT interval and the carboxyhemoglobin level was significant (P = 0.0072, R2 = 0.1017), as were the relationships between QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2358) and the corrected QT dispersion and carboxyhemoglobin (P < 0.001, R2 = 0.2613). The multivariate logistic analysis showed that the significant predictors of sequential disability were hyperbaric oxygen therapy (P = 0.0182), corrected QT dispersion (P = 0.0062), and troponin I level (P = 0.0002). Conclusions Patients’ prognosis following carbon monoxide poisoning can be predicted based on corrected QT dispersion and the troponin I level. Patients with myocardial damage should be monitored not only for their cardiovascular outcome but also for their neurological outcome and their prognosis.


2019 ◽  
Vol 38 (8) ◽  
pp. 974-982 ◽  
Author(s):  
N Dindar Badem ◽  
E Cömertpay ◽  
F Coşkun

Carbon monoxide (CO) is an important cause of deaths via poisoning. CO poisoning causes inhibition of O2 transport and development of tissue hypoxia, which then causes cell apoptosis. A significant indicator of cell apoptosis, soluble tumor necrosis factor-like weak inducer of apoptosis (sTWEAK) protein, is important for the stimulation of apoptosis. The primary purpose of this study is to determine whether apoptosis occurs during acute CO poisoning and to show that sTWEAK protein is an indicator of apoptosis that can be analyzed as a marker in the peripheral blood sample. The secondary aim is to determine the diagnostic and prognostic values of sTWEAK protein. The study was performed prospectively on 43 patients with CO poisoning and 30 healthy volunteer control individuals. The anamneses were taken from all patients, who also underwent physical examination. Complete blood count, biochemical markers, cardiac enzymes, and arterial blood gas measurements were analyzed. All the patients’ sTWEAK protein levels were also analyzed. The sTWEAK protein level of patients with CO poisoning was 2278 pg/mL (1197–7234), while the level of the control group was 1609 pg/mL (310–3721). The patients’ sTWEAK levels were significantly higher than the controls (area under the curve: 0.77 (0.66–0.89); p < 0.001), and the cutoff value was determined as 1895.50 pg/mL. The cutoff level had a sensitivity of 74.4%, a specificity of 76.7%, a positive predictive value of 82.0%, and a negative predictive value of 67.6%. sTWEAK is a significant indicator of apoptosis in CO poisoning that can be analyzed in the peripheral blood. However, further clinical trials are needed in terms of prognostic criteria.


Diagnostics ◽  
2020 ◽  
Vol 10 (4) ◽  
pp. 242 ◽  
Author(s):  
June-Sung Kim ◽  
Byuk Sung Ko ◽  
Chang Hwan Sohn ◽  
Youn-Jung Kim ◽  
Won Young Kim

Myocardial dysfunction due to acute carbon monoxide (CO) poisoning is common and associated with poor outcomes. The role of cardiac markers, including creatine kinase-myocardial band (CK-MB), high-sensitivity troponin I (hsTnI), and brain natriuretic peptide (BNP), in identifying patients with CO-induced cardiomyopathy were evaluated. This single-center, retrospective cohort study included 905 consecutive adult patients in the CO poisoning registry from February 2009 to December 2019. Cardiomyopathy was defined as any abnormality on transthoracic echocardiography (TTE), including left ventricular systolic and diastolic dysfunction, right ventricular dysfunction, and wall motion abnormalities. The areas under receiver operating curves (AUCs) for biomarkers were compared. Of the 850 included patients, 101 (11.9%) had CO-induced cardiomyopathy. Initial and peak hsTnI and CK-MB concentrations, and initial BNP concentrations were significantly higher in patients with than without cardiomyopathy (all P-values < 0.01), but the AUCs were higher for hsTnI (0.894) and CK-MB (0.864) than for BNP (0.796). Initial TnI > 0.01 ng/mL and CK-MB > 1.5 ng/mL each had 95% sensitivity and 97% negative predictive value for CO-induced cardiomyopathy. Higher hsTnI or CK-MB levels on admission can identify patients at high-risk of CO-induced cardiomyopathy and can be a screening tool for CO poisoning.


Author(s):  
Christos E Lampropoulos ◽  
Evagelia Sklavou ◽  
Charalampos Anastogiannis ◽  
Vasiliki Papanikolaou ◽  
Dimitris Tsilivarakis ◽  
...  

Introduction: Carbon monoxide (CO) poisoning may cause severe cellular hypoxia. Materials and methods: A 28-year-old male presented reduced levels of consciousness and dyspnoea after CO exposure. Clinical examination revealed tachypnoea, bilateral rales, dilated jugular veins and confusion. Troponin I, lactate and carboxyhaemoglobin levels were increased. Thoracic X-ray depicted pulmonary oedema and an echocardiogram, severe heart failure (HF; EF<25%). He was intubated due to clinical deterioration. Results: He remained intubated for 5 days with excellent improvement of left ventricular function (EF>55%). He was discharged 1 week later with full recovery. Discussion: Acute HF is a rare serious complication of CO poisoning, even in healthy young individuals.


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