Abstract
To determine if meconium in the amniotic fluid (AF) can cause cerebral palsy by stimulating umbilical and placental blood vessels to constrict. Brain injury patterns were analyzed in 43 children whose exposure to meconium in the AF was their only identified risk for quadriplegic cerebral palsy. The times their injuries occurred were established by following lymphocyte counts in their blood after birth. All 43 had cerebral cortical and subcortical brain damage of the type produced by late gestational ischemia and hypoxemia. The time between the onset of injury and birth ranged from 2-38 hours. The neonates were severely acidotic at birth when birth occurred within 12-14 hours after ischemia and hypoxemia began. Thereafter, the acidosis receded as the time between its start and birth increased, presumably because vasoconstriction had ended. Severe acidosis did not recede in nine children whose cerebral palsy was due to disorders that kept them hypoxemic until birth. Meconium in the AF may sometimes initiate vasoconstriction that leads to ischemic, hypoxemic cerebral palsy.
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