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Neonatal Encephalopathy

Jul 2010 – by M. Socol, MD

The advent of fetal heart rate monitoring fueled optimism that the incidence of cerebral palsy and mental retardation could be reduced by 50%. This hope, however, never came to fruition. The incidence of cerebral palsy has remained at approximately 2 per 1,000 births while the incidence of mental retardation is about twice as frequent. Clearly, the rising cesarean delivery rate over recent decades cannot be defended by any recognized improvement in neonatal neurologic outcome.

Cerebral palsy is defined as non-progressive motor spasticity of early onset. Although in our litigious society the obstetrician is often blamed for this untoward outcome, oxygen deprivation proximate to delivery appears to account for only 10% of cases of cerebral palsy. The single most important identifiable risk factor is preterm birth. In contrast, mental retardation, which is determined by IQ score, is most often related to chromosomal or congenital aberrations. Children with cerebral palsy are often also afflicted with mental retardation but the reverse is much less common.

Whether a severe asphyxial event affects a fetus, child, or adult, the human body responds by preferentially shunting blood to the brain, heart, and adrenal glands. Consequently, both physiologic experiments and clinical experience have identified a constellation of signs and symptoms that one would expect to observe if oxygen deprivation proximate to birth has occurred to the extent to cause hypoxic ischemic encephalopathy, or brain damage. This constellation includes low pH, depressed Apgar scores for a prolonged period of time, multiorgan dysfunction (eg, anuria, persistent fetal circulation, elevated liver enzymes, feeding difficulties), and central nervous system abnormalities (seizures, profound hypotonia, coma). It is important to remember that only one or two of these observations are not enough to support the diagnosis of "birth asphyxia."

The American College of Obstetricians and Gynecologists and the American Academy of Pediatrics have jointly published a monograph which enumerates the criteria that should be used to determine whether an acute intrapartum hypoxic event sufficient to cause cerebral palsy has occurred. These are divided into essential criteria and criteria that collectively suggest an intrapartum timing (within close proximity to labor and delivery, eg, 0-48 hours) but are nonspecific to asphyxial insults.

Essential criteria (must meet all four)

  • Metabolic acidosis in umbilical cord arterial blood (pH < 7.0 and base deficit ≥ 12 mmol/L)
  • Early onset of severe or moderate neonatal encephalopathy
  • Cerebral palsy of the spastic quadriplegic or dyskinetic type
  • Exclusion of other identifiable etiologies such as trauma, coagulation, disorders, infectious conditions, or genetic disorders

Suggestive, but nonspecific criteria

  • Sentinel hypoxic event occurring immediately before or during labor
  • Sudden and sustained fetal bradycardia or the absence of fetal heart rate variability in the presence of persistent late or variable decelerations, usually after a hypoxic sentinel event.
  • Apgar scores of 0-3 beyond 5 minutes
  • Onset of multisystem involvement within 72 hours of birth
  • Early imaging study showing evidence of acute nonfocal cerebral abnormality

References

Neonatal Encephalopathy and Cerebral Palsy. Copyright January 2003 by the American College of Obstetricians and Gynecologists.