Abstract

Background Neonatal hypoxic–ischemic encephalopathy (HIE) is a neonatal brain injury caused by perinatal asphyxia and is a major cause of neonatal morbidity and mortality. Cardiac dysfunction forms a part of the clinical spectrum of multiorgan dysfunction in asphyxiated newborns. The more cardiac dysfunction the patients have, the more severe encephalopathy they would suffer. Cardiac troponin I (cTnI) is one of neonatal HIE-related biomarkers that can aid the diagnosis of perinatal asphyxia and anticipate the severity of associated myocardial dysfunction. Aim The current study was designed to assess the serum cTnI concentration and to evaluate its short-term prognostic value in newborns with HIE. Patients and methods The present study is a prospective observational study conducted on 100 full-term newborn infants in the period from May 2016 to May 2017. Enrolled newborns were divided into two groups: the case group (50 full-term newborn infants with evidence of perinatal asphyxia) and the control group (50 full-term newborn infants without evidence of perinatal asphyxia). Quantitative estimation of serum cTnI concentrations was done in all enrolled newborns within 12 h of birth using direct chemiluminometric technology performed on ADVIA Centaur Immunoassay System (TnI-Ultra). Serum levels of creatine kinase-MB (CK-MB) were also measured to assess its sensitivity and specificity as a marker of perinatal asphyxia. Additionally, echocardiography was done to exclude structural heart diseases. Left ventricular fractional shortening (LVFS) was also measured to assess cardiac involvement. Results Serum concentrations of cTnI were statistically significantly higher among the case group when compared with the control group. Additionally, serum levels of cTnI were found to increase with increasing severity of HIE. Serum levels of CK-MB were also statistically higher among the case group. However, pairwise statistical comparison of serum CK-MB concentrations in different stages of HIE revealed no statistical significant difference. No statistical significant difference was found between the two studied groups regarding LVFS. Moreover, LVFS did not differ significantly between the different stages of HIE. Among the different markers of myocardial dysfunction assessed in the current study, cTnI was found to be the most sensitive and specific predictor of poor short-term outcome in newborns with perinatal asphyxia. When comparing serum concentrations of cTnI and CK-MB in both surviving and nonsurviving newborns in the asphyxia group, it was found that serum concentrations of cTnI were statistically significantly lower in the group of survivors. In contrast, there was no statistical significant difference regarding serum concentrations of CK-MB between surviving and nonsurviving asphyxiated newborns. Conclusion Serum concentrations of cTnI were elevated in asphyxiated newborns with respect to healthy infants and increase with increasing severity of HIE. cTnI can also be used as an excellent early predictor of mortality in newborns with perinatal asphyxia.

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