Doppler evaluation of brainstem flow in asphyxiated neonates with delayed auditory brainstem evoked responses

Background. In animals, it has been demonstrated that asphyxia leads to transient ischemia and reperfusion of the brain. As a consequence of reperfusion, there is free-radical mediated neural damage, and progressive hypoperfusion of the brain lasting for approximately one week after the event. Studies using positron emission tomography have corroborated these findings in human neonates. The sonographic/Doppler findings during the phase of hypoperfusion have thus far not been characterized. Also, delayed auditory brainstem evoked responses (ABRs) have been documented in asphyxiated neonates in the first few days of life. The association of altered brainstem flow with delays in ABR component latencies has thus far not been studied.; Methods. ABRs were recorded and pulsatility indices in the basilar artery and branches of the middle cerebral artery were measured using the Doppler technique in 40 neonates admitted to the neonatal intensive care unit (NICU). A ratio of brainstem to cortical impedance was computed. Asphyxia was defined on the basis of arterial blood gases. Neurological outcome at discharge was based on evaluation by an independent pediatric neurologist.; Results. We found that asphyxiated neonates had higher basilar to middle cerebral artery impedance ratios. Higher ratios were associated with delayed ABR wave III component latencies as well as poor neurological outcome during hospital stay. In asphyxiated neonates, high impedance and low-flow states in the basilar territory were significantly associated with higher ratios.; Conclusions. Asphyxia causes delayed low-flow states in the basilar territory, that are associated with delayed ABR component latencies and impaired neurological outcomes.