Abstract
In the first days after birth, a major focus of research is to identify infants with hypoxic-ischemic encephalopathy at higher risk of death or severe neurological impairment, despite therapeutic hypothermia (TH). This is especially crucial to consider redirection of care, according to neonatal outcome severity. We aimed to seek associations between some neonatal routine parameters, usually recorded in Neonatal Intensive Care Units, and the development of severe outcomes. All consecutive patients prospectively recruited for TH for perinatal asphyxia, born between February 2009 and July 2016, were eligible for this study. Severe outcome was defined as death or major neurological sequelae at one year of age. Among all eligible neonates, the final analysis included 83 patients. Severe outcome was significantly associated with pH and base excess measured in the first hour of life, mode of delivery, Apgar score, Sarnat and Sarnat score, electroencephalogram-confirmed neonatal epileptic seizures, and antiepileptic therapy. Studying univariate analysis by raw relative risk (RR) and 95% confidence intervals (CI), severe outcome was significantly associated with pH (p = 0.011), Apgar score (p = 0.003), Sarnat score (p < 0.001), and Caesarian section (p = 0.015). Conclusions. In addition to clinical examination, we suggest a clinical-electroencephalographic protocol useful to identify neonates at high neurological risk, available before rewarming from TH.
Highlights
Hypoxic Ischemic Encephalopathy (HIE) is a neonatal neurological syndrome characterized by central nervous system depression, seizures, and abnormal electroencephalogram (EEG)
It is caused by perinatal asphyxia that leads to metabolic acidosis and low Apgar scores [2,3,4]
Neonatal parameters were not significantly different in those infants born by cesarean section compared to others, except at 1 min (p = 0.001) and 5 min (p = 0.01) Apgar score
Summary
Hypoxic Ischemic Encephalopathy (HIE) is a neonatal neurological syndrome characterized by central nervous system depression, seizures, and abnormal electroencephalogram (EEG). Reported incidence is 1–2/1000 newborns [1]. It is caused by perinatal asphyxia that leads to metabolic acidosis and low Apgar scores [2,3,4]. The HIE is classified according to the severity of encephalopathy using the Sarnat and Sarnat score, which is based on clinical signs and EEG alterations [5]. The cerebral damage is produced through three different phases: a potentially reversible primary phase, a latency phase, and a phase of irreversible secondary damage leading to cellular death, starting from the 6th to the 15th hour [6]. A therapeutic window allows intervention with hypothermic treatment
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