The effect of full blood count and cardiac biomarkers on prognosis in carbon monoxide poisoning in children

Abstract

Aims In this study, cardiac biomarkers, blood parameters, electrocardiography (ECG), and echocardiography were investigated in children with carbon monoxide (CO) poisoning, and the diagnostic value of these parameters was investigated. Methods The demographical, clinical, and laboratory data of children aged 0–18 years who were admitted to the pediatric emergency department due to CO poisoning between January 2019 and January 2022 were retrospectively scanned from medical records. The patients were divided into two groups as troponin-I positive and troponin-I negative. Results There were 107 children aged 0–18 years (average age, 10.46 ± 5.77 years; 51% female) with CO poisoning. There were 13 patients with troponin-I positive myocardial injury. Troponin-I was positive in 3 patients whose carboxyhemoglobin (COHb) level was below 2% at the time of admission. In one patient, troponin-I, which was normal at admission, increased by the 24th hour of hospitalization. Hyperbaric oxygen therapy was given due to headache in one patient, although the COHb level of that patient was below 25%. An NT-proBNP level of ≥ 219.5 ng/L predicted the development of troponin-I positivity with a sensitivity of 70% and a specificity of 86.7% (AUC, 0.967 (0.58–0.994); p = 0.017). White blood cell (WBC), neutrophil, neutrophil-to-lymphocyte ratio (NLR), immature granulocyte (IG), and IG% levels were found to be significantly higher in the troponin-positive patient group. Discussion and conclusion NT-proBNP has been shown to be an early diagnostic marker for myocardial dysfunction. Additionally, when cardiac markers are not available, full blood parameters may assist clinicians for patient treatment and referral.

A patient with toxic encephalopathy associated with acute carbon monoxide poisoning–A clinical case

“…Cardiovascular complications caused by CO poisoning have mostly been reported as left ventricular dysfunction, arrhythmias, and pulmonary edema, but it can also induce a coronary spasm and intracoronary thrombosis, leading to acute coronary syndrome even in healthy patients and in ones with non-critical atherosclerotic plaques. Some patients may have ST depressions or T wave inversions [8][9][10][11].…”