++
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.
++
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.
++
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
++
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 ...