And what about cord blood cardiac troponin i (cTnI) levels as an inclusion criterion for therapeutic hypothermia after perinatal asphyxia?

摘要

Hypoxic-ischemic injury remains a major cause of perinatal death and permanent neurological deficits worldwide (1,2). Induced hypothermia with total body cooling seems to provide neuroprotection in infants having encepha-lopathy that follows an acute moderate-severe hypoxic ischemic insult at birth, accounting for a favorable effect on multiple pathways contributing to brain damage (2). Therapeutic hypothermia has been reported to be safe and effective in reducing the rate of death and in preventing neurodevelopmental disability in this high-risk population (1). It involves the controlled reduction of core temperature to attenuate the secondary organ damage that occurs after a primary injury (3). Babies must meet both physiologic and neurologic criteria for total body hypothermia (1, 2). Treatment with hypothermia should be offered to neonates within 6 h after birth who are born at >36 weeks' gestation and with birth weight of >1800 g and who show clinical signs of moderate to severe neonatal encephalopathy as well as evidence of hypoxia-ischemia, i.e., 10-min Apgar score <5, need for resuscitation at 10 min, blood pH <7.00, or base deficit > 16 mmol/L (1-3). The potential of using biomarkers for early detection of the initial hypoxia-ischemia is of huge utility to more precisely target infants who will go to develop clinically significant neurological sequelae, delivering therapeutic hypothermia only to newborns who would benefit from it. Myocardial dysfunction is a common complication of perinatal asphyxia (4). Cardiac troponin I (cTnl) is considered a highly specific indicator of myocardial ischemic damage in adults (5, 6).