Fetal hypoxic and ischemic injuries.

PURPOSE OF REVIEW

The principles of neonatal neurological protection following intrapartum hypoxia are briefly reviewed. The physiological principles behind the use of cardiotocograph patterns in defining the timing and mechanism of fetal hypoxia and injury are then demonstrated.

RECENT FINDINGS

Fetal neurological injury may result from progressive hypoxemia, acidosis, diminished cardiac output and cerebral ischemia, manifested at birth as low Apgar scores, multisystem compromise, severe acidosis and encephalopathy. More commonly, however, intrapartum injury results from often intermittent, regional ischemia secondary to umbilical cord or head compression resulting in hemorrhage or infarction. Under these circumstances, the amount of umbilical acidosis and neonatal encephalopathy varies and the potential candidate for neuroprotection may escape recognition and timely treatment. Selecting infants likely to benefit from neuroprotection requires information on the timing, duration and mechanism of hypoxia. Neonatal parameters, including low Apgar scores, acidosis, even seizures, lack sensitivity and specificity. Cardiotocograph patterns are capable of determining the duration, mechanism and severity of hypoxia and occasionally, the timing of neurological injury.

SUMMARY

Protecting the newborn from the neurological consequences of intrapartum hypoxia requires critical definition of the mechanism and timing of this exposure. cardiotocograph tracings offer the opportunity to refine the selection of candidates for neonatal rescue.