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Neonatal encephalopathy is a clinically defined syndrome of disturbed neurological function in the early postnatal days of life in the term infant, manifested by a combination of signs including altered consciousness, abnormal muscle tone or reflexes, altered respiration or seizures. Etiologies of neonatal encephalopathy include the combination of intrapartum or antepartum hypoxia and ischemia (hypoxic-ischemic encephalopathy), which may be accompanied by some prenatal signs of fetal distress; vascular pathologies, including intracranial bleeding and stroke; injuries secondary to birth trauma; infections; genetic and metabolic disorders; and congenital brain abnormalities. This chapter is focused on brain injuries and abnormalities in term newborn infants, with particular emphasis on infants who present with biochemical and clinical evidence of hypoxic-ischemic encephalopathy, and the current diagnostic and treatment approaches to such injury. Other birth injuries associated with central nervous system damage including vascular malformations and birth trauma are briefly discussed as well.

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Neonatal encephalopathy occurs in 1 to 6 per 1000 live full-term births, with a recent population-based estimate of 1.9 to 3.8 per 1000.1 Fifteen to 20% of affected newborns will die in the postnatal period, and an additional 25% will sustain childhood disabilities.2 Neonates with mild encephalopathy do not have an increased risk of motor or cognitive deficits. Neonates with severe encephalopathy have an increased risk (> 60%) of death or of cerebral palsy and mental retardation. Neonates with moderate encephalopathy have a higher likelihood of death or deficits, such as memory impairment, visual motor or visual perceptive dysfunction, increased hyperactivity, and delayed school readiness, that is approximately half that of those with severe encephalopathy.

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The cause and timing of such injuries is usually unknown. Since neonatal encephalopathy has myriad causes, diagnostic criteria that suggests a hypoxic-ischemic insult is attributable to an acute intrapartum event has been suggested. These include metabolic acidosis with a cord pH below 7 or a base deficit of 12 mmol/L or greater, early onset of encephalopathy, and exclusion of another etiology such as trauma, coagulation disorder, and genetic and metabolic causes. Infants with severe injury and hypoxic-ischemic encephalopathy related to an intrapartum event develop either spastic quadriplegia or dyskinetic type cerebral palsy. Signs consistent with an event in the 48 hours prior to delivery, but not necessarily an acute event, include a sentinel event occurring immediately before or during labor; a sudden sustained fetal bradycardia or absence of fetal heart rate variability in the presence of persistent, late, or variable decelerations, usually after a sentinel event before which the fetal heart rate pattern was normal; Apgar scores less than 3 at 5 minutes; multisystem organ involvement apparent within 72 hours of birth; and early imaging studies demonstrating evidence of acute nonfocal cerebral abnormalities.3

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The vast majority of infants with encephalopathy do not have an identifiable intrapartum event such as cord prolapse or uterine rupture.4 Although there is no specific diagnostic test for hypoxic-ischemic encephalopathy, neuroimaging studies identifying injury to the basal ganglia and parasagittal ...

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