ASSOCIATION OF HIGH SENSITIVITY CARDIAC TROPONIN I LEVELS IN NEW BORN WITH BIRTH ASPHYXIA IN PREDICTING EARLY MYOCARDIAL INJURY - A ONE YEAR HOSPITAL BASED CASE CONTROL STUDY

Perinatal asphyxia is one of the leading causes of early neonatal mortality and according to WHO it accounts to estimated 900,000 deaths worldwide each year. The ICD-10 WHO definition of birth asphyxia as failing to initiate and sustain breathing at birth is specified by the two categories of codes: P20 “intrauterine hypoxia” and P21 “birth asphyxia”.

·       In India, the incidence of perinatal asphyxia is as high as 8.4% (considering the definition of birth asphyxia as Apgar score of < 7 at 1 min). Perinatal asphyxia is one of the leading causes of neonatal mortality (28%) in our country and it is the most common and important cause of preventable cerebral injury occurring in the neonatal period.

·       Neonatal asphyxia results in low foetal tissue perfusion, hypoxic ischemic injury, hypercapnia, and acidosis and is potentially fatal. survivors from neonatal asphyxia can suffer from morbidities such as motor and cognitive deficits that originate from cerebral hypoxia ischemia.

Troponin, a protein complex consisting of I, T and C subunits, is located at the actin filaments of the myocardium and is essential for calcium-mediated muscle contraction. Troponin I and T are cardiac-specific subunits and markers of myocardial damage.

·       several studies have demonstrated that troponin-I is a good marker of myocardial dysfunction and early death in infants with HIE.

·       Troponin I levels in the blood are very low (<30 pg/ml in newborns) but injuries to the heart can cause the levels to increase significantly. Troponin I is a commonly used cardiac biomarker that may be useful for determining whether patients have perinatal asphyxia.

·       The early diagnosis of the myocardial injury can limit the mortality associated with neonatal asphyxia.

·       Aim of the study is to estimate the levels of high sensitivity cardiac troponin I in newborns with birth asphyxia and to correlate the findings with echocardiography.

·       In patients with perinatal asphyxia, cardiac output is directed from less vital organs (liver, kidneys, and intestines) toward more critical organs such as the brain, heart, and adrenal gland due to hypoxia.

·       Bradycardia develops rapidly with acute hypoxia and persists as acidosis becomes more severe; blood pressure is normal at this stage due to peripheral vasoconstriction and the redistribution of cardiac output toward vital organs.

·       If asphyxia continues, blood pressure drops, and ischemia occurs in the vital organs. low heart rate due to asphyxia and acidosis and the subsequent decrease in myocardial contractility due to ischemic cardiac injury reduce ventricular output and stroke volume. with reduced cardiac output, coronary perfusion decreases, and myocardial damage occurs.