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Ann Thorac Surg 2001;71:877-880
© 2001 The Society of Thoracic Surgeons


Original article: cardiovascular

Time course of cranial ultrasound abnormalities after arterial switch operation in neonates

Matthias Sigler, MDa, Jaime F. Vazquez-Jimenez, MDb, Ralph G. Grabitz, MDa, Hedwig H. Hövels-Gürich, MDa, Bruno J. Messmer, MDb, Götz von Bernuth, MDa, Marie-Christine Seghaye, MDa

a Department of Pediatric Cardiology, Aachen University of Technology, Aachen, Germany
b Department of Thoracic and Cardiovascular Surgery, Aachen University of Technology, Aachen, Germany

Accepted for publication August 21, 2000.

Address reprint requests to Dr Sigler, Klinik für Kinderkardiologie, Pauwelsstr 30, D-52057 Aachen, Germany
e-mail: matthias.sigler{at}post.rwth-aachen.de

Background. The object of this study was to investigate the time course and fate of abnormal findings in cranial ultrasound after performing an arterial switch operation in neonates with transposition of the great arteries, and to analyze the relationship to cerebral cell damage.

Methods. Cranial ultrasound was performed prospectively in 35 neonates with transposition of the great arteries before the operation as well as 4 hours, 1, 2, and 3 days, and 1 and 2 weeks postoperatively. Blood levels of neuron-specific enolase, a marker of cerebral cell damage, were determined before, during, and 4 and 24 hours postoperatively.

Results. In 17 of 35 neonates (49%), early postoperative cranial ultrasound revealed abnormalities indistinguishable from intraventricular hemorrhage. In 11 neonates findings were transient and were normalized 2 weeks postoperatively, whereas in the remaining 6 neonates there was evidence of resolving hemorrhage. In all neonates there was a rise in neuron-specific enolase blood concentrations during and 4 hours after extracorporal circulation without correlation to sonographic findings.

Conclusions. Enhanced echogenicity of the choroid plexus or dilatation of the cerebral ventricular system is a frequent early postoperative finding that may be caused by transient plexus edema rather than intraventricular hemorrhage and is not related to cerebral cell damage.




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