Key result
Severe neonatal asphyxia is linked to ~8-fold higher cardiac troponin-I levels versus healthy controls.
Why the study?
Cardiac dysfunction in perinatal asphyxia can cause severe outcomes, and ECG and cardiac enzyme levels can demonstrate impaired myocardial function.
Does the severity of birth asphyxia correlate with ECG changes and cardiac troponin-I levels in full-term neonates?
Case-Control (n=60)
No
Does the severity of birth asphyxia correlate with ECG changes and cardiac troponin-I levels in full-term neonates?
Cardiac troponin-I levels and ECG changes correlate linearly with the severity of birth asphyxia, suggesting their utility in predicting outcomes in perinatal asphyxia.
cTnI elevation tracks asphyxia severity in neonates; leaves open its value as routine prognostic marker pending prospective validation.
Introduction: Cardiac dysfunction is well known in perinatal asphyxia caused by transit myocardial ischemia. Sometimes cardiac dysfunction may be so severe that it can cause congestive cardiac failure and shock that leads to death of newborn. ECG and serum levels of cardiac enzymes can be used to demonstrate impaired myocardial function. Material and Methods: It was a case control study conducted in the department of paediatrics, Gandhi Medical College, Bhopal over a period of 12 months from January 2013 to December 2013. Forty asphyxiated full term neonates were taken as cases and 20 healthy full term neonates as controls. Forty neonates with asphyxia admitted to NICU with gestational age >37 completed weeks and with birth weight >2 kg taken as cases and twenty healthy full term neonates (37 completed wks) unasphyxiated weighing >2 kg at birth with clear liquor and 1 min Apgar score >7. Results: Myocardial dysfunction was present in 90% of the newborns with severe birth asphyxia and 40% of newborns with moderate birth asphyxia. T wave changes were seen in 80% neonates with severe asphyxia and 33% neonates with moderate asphyxia. In present study, cTn I levels in severely asphyxiated neonates were significantly higher than moderately asphyxiated neonates and control group neonates (4.6 ng/ml, range 2.1 – 7.8, and 1.8 ng/ml, range 0.2 – 4.8 ng/ml and 0.6ng/ml, range 0.2-1ng/ml respectively). Conclusion: We found a linear relationship between levels of cardiac troponin-I and birth asphyxia. Therefore cardiac troponin-I level may be useful in predicting the mortality and outcome in perinatal asphyxia.
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Pal et al. (2015) conducted a case-control in Birth asphyxia (n=60). Birth asphyxia vs. Healthy unasphyxiated neonates was evaluated on Cardiac troponin I (cTn I) levels (p=<0.005). Cardiac troponin-I levels were significantly higher in severely asphyxiated neonates (4.6 ng/ml) and moderately asphyxiated neonates (1.8 ng/ml) compared to healthy controls (0.6 ng/ml, p<0.005).
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