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Acute cardiac effects of carbon monoxide poisoning in children
Ozlem Teksam1, Pinar Gumus, Benan Bayrakci
1Department of Pediatrics, Hacettepe University School of Medicine, Ihsan Dogramaci Children's Hospital, Sihhiye, Ankara 06100, Turkey. ozlemt@hacettepe.edu.tr
Insights
Carbon monoxide (CO) poisoning can cause heart damage in children, even without abnormal ECGs. Low Glasgow Coma Scale (GCS) scores and hypotension are linked to this myocardial injury.
Area of Science:
- Pediatric Cardiology
- Toxicology
- Emergency Medicine
Background:
- Carbon monoxide (CO) poisoning is a rare cause of cardiotoxicity in children.
- Existing reports are limited to isolated case studies.
- Acute cardiac effects and myocardial injury in pediatric CO poisoning require further investigation.
Purpose of the Study:
- To describe the acute cardiac effects in children with CO poisoning.
- To identify factors associated with myocardial injury in pediatric CO poisoning cases.
Main Methods:
- Retrospective review of medical records for children (<17 years) with CO poisoning (carboxyhemoglobin ≥10%).
- Analysis of cardiac biomarkers (creatine kinase-MB, troponin-t), ECG, and echocardiography findings.
- Correlation of myocardial injury with clinical factors like Glasgow Coma Scale (GCS) and hypotension.
Main Results:
- 15% (16/107) of pediatric CO poisoning patients showed myocardial injury via elevated cardiac biomarkers.
- Sinus tachycardia was observed in 32% of patients; no ischemic ECG changes were noted.
- Echocardiography revealed low ejection fraction and abnormal left ventricular function in 9 of 27 patients.
Conclusions:
- Myocardial injury can occur in pediatric CO poisoning without abnormal ECG findings.
- A Glasgow Coma Scale (GCS) score ≤14 and hypotension are significant risk factors for myocardial injury.
- These findings highlight the importance of cardiac monitoring in children with CO poisoning.
Objective:
Carbon monoxide (CO)-induced cardiotoxicity has been investigated infrequently in children and reports of its cardiovascular effects are limited to isolated case reports. Our aims were to describe acute cardiac effects and associated factors with myocardial injury in children with CO poisoning.
Methods:
We reviewed the medical records of children below 17 years of age who were diagnosed with CO poisoning at pediatric emergency department between July 2004 and June 2007. Patients who had carboxyhemoglobin level at least 10% were included. Myocardial injury was defined as elevated cardiac biomarkers (creatine kinase-MB or troponin-t). Carboxyhemoglobin level, electrocardiogram (ECG) findings, cardiac biomarkers, and echocardiograph results were recorded for each patient.
Results:
Cardiac biomarkers were drawn in 107 patients, of which 16 patients (15%) had cardiac biomarkers confirmed diagnosis of myocardial injury. Sinus tachycardia was present in 32% of patients on baseline ECG. None of the patients had ischemic changes on ECG. Echocardiograph was performed in 27 patients (25% of patients with biomarkers drawn), of which nine patients had low ejection fraction and abnormal left ventricular function. Determinators of myocardial injury included a Glasgow Coma Scale (GCS) score
Conclusion:
Myocardial injury may exist in children with CO poisoning without abnormal ECG findings. GCS score
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