Volume 3 Supplement 2
International Symposium on the Pathophysiology of Cardiopulmonary Bypass
Value of cranial ultrasound for diagnosing neuronal cell damage during arterial switch operation (ASO) in neonates with transposition of the great arteries (TGA)
© Current Science Ltd 1999
Published: 2 March 1999
To assess the reliability of cranial ultrasound in diagnosing neuronal cell damage after the ASO in neonates.
Cranial ultrasound was prospectively performed in 35 neonates with TGA before the operation as well as 4 h, 1, 2, 3 days, 1 and 2 weeks postoperatively (po). Blood concentrations of neuron specific enolase (NSE), a marker of neuronal cell damage, were determined before, during as well as 4 and 24h po. The ASO was performed under combined low-flow cardiopulmonary bypass and hypothermic circulatory arrest.
Areas of enhanced echogenicity in the choroid plexus and the ventricular system were seen in one newborn before the ASO, whereas 17 of 35 (49%) showed po enhanced echogenicity not distinguishable from intraventricular hemorrhage (IVH) I° to III°. No other abnormalities were seen intracranially before or after the operation. In 11 neonates findings were only temporary with normal scans 2 weeks po, while in the other 6 there was evidence of resolving hemorrhage. Also retrospectively, it was not possible to distinguish the findings in neonates with and without early signs of IVH during the first week po. In all neonates there was a significant rise in NSE blood concentrations during and 4 h after extracorporal circulation when compared to preoperative values (P < 0.005). No significant correlation was observed between NSE levels and occurrence of intracranial enhanced echogenicity during or after the ASO. NSE blood concentrations, however, were correlated to the occurrence of po seizures (P < 0.05).
Our data show that the presence of po enhanced echogenicity in the cerebral ventricular system of neonates with TGA after ASO is not correlated with neuronal cell damage. We speculate that enhanced echogenicity seen in cranial ultrasound is caused more likely by plexus edema than by intraventricular hemorrhage.