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ESSENTIALS OF DIAGNOSIS AND TYPICAL FEATURES
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ESSENTIALS OF DIAGNOSIS AND TYPICAL FEATURES
Neonatal encephalopathy is a clinical condition in the first days after birth manifested by alterations in consciousness, hypotonia, seizures, abnormal reflexes, and apnea.
Hypoxic-ischemic injury in the peripartum period is the most common cause of neonatal encephalopathy and is referred to as hypoxic-ischemic encephalopathy (HIE).
The diagnosis of neonatal HIE is based on multiple clinical and laboratory criteria, including Apgar scores, clinical appearance of the neonate, acidosis, multiorgan injury, and characteristic patterns of brain injury on magnetic resonance imaging (MRI).
Moderate to severe neonatal HIE carries a high risk of death and disability.
Therapeutic hypothermia is the standard of care for neonatal HIE in term infants and has been shown in multiple large trials to reduce risk of death and disability at 18 months and beyond.
HIE is more common in preterm than in term infants, but there is no treatment with enough evidence to recommend as standard of care for preterm infants with HIE.
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GENERAL CONSIDERATIONS
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Neonatal encephalopathy is a term defined by the American College of Obstetricians and Gynecologists as “a clinically defined syndrome of disturbed neurologic function in the earliest days of life in an infant … manifested by a subnormal level of consciousness or seizures, and often accompanied by difficulty with initiating and maintaining respiration and depression of tone and reflexes.”1 Hypoxic-ischemic injury in the peripartum period is the most common cause of neonatal encephalopathy, and this chapter will focus on diagnosis and management of HIE. HIE is caused by failure of perfusion to the fetal brain due to uterine, placental, or umbilical cord compromise prior to or during delivery.
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Hypoxic-ischemic injury as a cause of neonatal encephalopathy is often assumed, rather than certain, because few infants with encephalopathy have a known sentinel event such as placental abruption or cord prolapse.2 Often, hypoxic-ischemic injury can be assumed without knowledge of a sentinel event in encephalopathic neonates in the presence of low Apgar scores, acidosis, and acute brain injury seen on MRI, or it may be diagnosed retrospectively in an older infant or child with cerebral palsy and MRI evidence of brain injury in a pattern typical of hypoxic-ischemic injury.
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The pathologic events of hypoxic-ischemic injury occur in 2 phases, primary energy failure and secondary energy failure, between which there is a latent phase that presents a window of opportunity for intervention.3 Primary energy failure occurs as a result of the initial reduction of cerebral blood flow. Decreased cerebral blood flow leads to decreased availability of oxygen and glucose, which in turn leads to decreased production of adenosine triphosphate (ATP) and increased production of lactate.4 Low ATP levels cause failure of many of the mechanisms that maintain cell integrity. Massive depolarization of neurons leads to release of excitotoxic neurotransmitters.5 Eventually this pathway leads ...