A PROSPECTIVE STUDY ON CARDIAC TROPONIN I AND ECG CHANGES IN DIAGNOSIS OF MYOCARDIAL INJURY DUE TO PERINATAL ASPHYXIA IN TERM NEONATES

Abstract

Perinatal asphyxia is the commonest cause of preventable cerebral injury among neonates. Birth asphyxia is a multi – system disorder with consequence that extend beyond the central nervous system . Reduced tissue perfusion, hypoxic ischemic injury, acidosis, hypercapnia, and brain injury are all symptoms of birth asphyxia, overall being potentially fatal. Asphyxiated neonates who survive can have co-morbid condition, like motor as well as cognitive deficits originating from cerebral hypoxic-ischemia. The most important cause of neonatal mortality related to hypoxic-ischemia is myocardial damage; there is significant myocardial morbidity among survivors. Myocardial injury occurs at a rate of 28–73 percent in neonates with hypoxia, and cardiac impairment is frequently ignored due to a lack of appropriate diagnostic tests. It is important to identify myocardial injury as early as possible by using specific marker like cardiac troponin I and ECG change in diagnosis of myocardial damage, hence this study was carried out. Objectives: 1. To measure the serum cardiac troponin I levels in asphyxiated term neonates. 2. To record the ELECTROCARDIOGRAPHIC changes in asphyxiated term neonates. 3. To find the association of cardiac troponin I levels and ECG changes in diagnosis of myocardial injury in asphyxiated term neonates. xiii Material and Methods : A prospective study included 50 neonates born at term with the evidence of birth asphyxia. Detailed perinatal history, Clinical systemic examination, Laboratory investigations, Neonatal ECG Electrode Placement and ECG findings were recorded. cTni and ECG was done at 6 hours and repeated at 12 to 24 hours. The outcomes measures were serum cTnI levels, ECG changes and mortality due to myocardial injury. Data analysis : The data entry was done in the Microsoft EXCEL spread sheet and the final analysis was done with the use of Statistical Package for Social Sciences (SPSS) software, IBM manufacturer, Chicago, USA, ver 21.0. Results: Mortality was seen in 6 out of 50 neonates (12%). ECG showed abnormalityin 34 cases. The levels of cTnI increased from the initial hours with values of 1.98 at 6hours and 2.47 at 12 to 24 hours showing that the values are increased in perinatal asphyxia. For initial 6 hours, cardiac troponin I cut-off values of >1.28 significantlypredicted ECG changes with 100% accuracy. Moreover, cardiac troponin I showed increasing trend with grade of ECG abnormality (grade 1 vs. grade 2 vs. grade 3 vs. grade 4: 1.97 vs. 2.33 vs. 3.52 vs. 3.92, p<0.0001). Even at 12-24 hours, cardiac troponin I cut-off of >1.82 significantlypredicted ECG abnormality with 100% accuracy. xiv  Moreover, cardiac troponin I showed a significant increasing trend with grade of myocardial injury (grade 1 vs. grade 2 vs. grade 3 vs. grade 4: 2.35 vs. 2.93 vs. 4.07 vs. 4.3, p<0.0001). Mean cardiac troponin I within 6 hours (ng/mL) was significantly higher in died patients than discharged (3.76±0.3 vs. 1.58±1.04, p<.0001).  Mean cardiac troponin I at 12 to 24 hours (ng/mL) in died patients was significantly higher than discharged (4.22±0.17 vs. 2.05±1.16, p<.0001). Conclusion: Cardiac troponin levels significantly increase during neonatal asphyxia. Receiver operative characteristic curve (ROC ) analysis showed that troponin I can be a useful diagnostic marker for myocardial injury at 6 hours with the cut off of more than 1.28 and at 12 to 24 hours with the cut off of more than 1.82, in patients with neonatal asphyxia. Moreover, cardiac troponin I was also associated with increasing grade of myocardial injury as shown by ECG changes. Hence our study concludes that elevated cardiac troponin I and its association with ECG changes can be a useful diagnostic marker of myocardial injury due to perinatal asphyxia. However further large multi centric trials are needed to validate it as standard diagnostic tool in the management of asphyxiated neonates