As such various demographic data such as gender, birth weight, length, head circumference, maternal registration status, gestational age, antenatal complications, obstetric problems, maternal age and weight were evenly distributed among different stages of HIE.
Meconium stained amniotic fluid was present in 50% of cases which is similar to the finding of Martin-Ancel et al. . Modes of delivery and meconium staining of liquor did not affect the progression to different stages of HIE in neonates with birth asphyxia.
Apgar score at 1 minute was <3 in 14(23.3%) and 3–5 in 46(76.7%) neonates. Apgar score at 5 minute was 3 to 5 in 57(95%) and >5 in 3(5%) cases. In a study by Shah et al. , Apgar score at 5 minute was less than 5 in (63.12%) neonates. Martin-Ancel et al.  also reported Apgar score at 1 minute was 4 in 70% of cases which is similar to our study. However, Apgar scores at 5 minute were ≥7 in 46%, 4 to 6 in 37%, and ≤ 3 in 14% of patients which is in contrast to our findings. In our study, 41(68.3%) neonates had seizures. Shah et al4 documented seizures or coma in 87% of cases.
The various clinical features related to cardiac dysfunction documented were respiratory distress, congestive cardiac failure and shock. We found respiratory distress in 32(53.3%) and shock in 29(48.3%) cases. One neonate had congestive cardiac failure which was present in HIE stage III group. Rajakumar et al. , reported respiratory distress in 20 (66.7%), cardiac failure in 11 (36.7%) and cardiogenic shock in 5 (16.7%); while 8 babies were asymptomatic. However, Mandal et al.  found congestive cardiac failure in higher percentage (36%) of their cases. They found shock in 44%, which is similar to our observation.
Pulmonary infiltrates suggestive of meconium aspiration were present in X-ray chest of 11(18.3%) neonates and of these, 9 cases belonged to severe HIE. ECG changes were present in 46(76.7%) neonates. Grade 1 ECG changes were seen in 19(41.30%), grades 2 and 3. in 13(28.26%) cases each. Rajakumar et al.  reported ECG changes in almost similar percentage (73.3%) of cases. The most common finding in their study was ‘T’ wave inversion (36.7%) followed by ‘T’ wave flattening (33.3%), which is equivalent, to grade 1 ECG change. These ECG abnormalities indicate myocardial ischaemia due to birth asphyxia in neonates.
Mean CK total level, CK MB and troponin I were 1176.8 IU/l, 147.5 IU/l and 1.4 ng/ml, respectively. Mandal et al.  and Warburton et al  reported CK-MB values as high as a 823.5 IU/l and 328 IU/l, respectively. Rajakumar et al  reported lower mean CK-MB level (121 IU/l) in their study. The enzyme levels showed significant rise with increasing severity of HIE; indicating more myocardial ischaemia in severe HIE than mild and moderate cases.
Primhak et al  studied serial electrocardiogram and CK-MB in term infants and found that CK-MB was associated with myocardial injury in asphyxiated infants. However, Omokhodion et al  concluded that specificity of CK-MB as a marker of myocardial injury in asphyxiated newborns is possible but remains uncertain. Borke and co-workers  showed cardiac troponin I to be a reliable marker of myocardial necrosis. Thus previous studies showed that perinatal asphyxia is associated with myocardial dysfunction. However, they did not provide information regarding interventions performed in the delivery room and moreover study was conducted prior to the introduction of standardized neonatal resuscitation ..
The influence of hypoxemia related myocardial dysfunction in the newborn occurs in 30% of asphyxiated neonetes  and is thought to be secondary to direct effect of ischaemia on cardiac myocytes. Enzymatic indicators of myocardial injury in the asphyxiated newborns are elevated and often associated with electrocardiographic changes. The measurement of cardiac troponin I may have a role in the early identification of neonates with myocardial damage secondary to ischaemia. However, cardiac abnormalities often are under diagnosed and require a high index of suspicion.
We found a clear relationship between outcome of asphyxiated newborns and alterations in ECG and enzymatic parameters as significantly higher proportions of non- survivors had ECG abnormalities and raised levels of CK-MB and troponin I. Patients showing more severe hypoxic damage also reflected the striking changes in these parameters. Hypoxia is responsible for multiorgan dysfunction causing deaths, but particularly results in myocardial damage despite ``preferential'' myocardial perfusion [5, 21]. These markers may be useful in providing appropriate cardiovascular support in addition to managing the primary condition.
Thus, it can be concluded that myocardial dysfunction secondary to perinatal asphyxia is more frequent than thought, for which it will be useful to submit asphyxiated neonates to ECG monitoring and assay of cardiac enzyme markers complemented with clinical findings. The early detection and prompt treatment of condition will help in improving prognosis of these asphyxiated newborns.