Improving neurological outcomes following neonatal cardiopulmonary bypass

Abstract

Subtle neurological complications are alarmingly frequent following surgical repair of congenital heart disease.  Periods of ischaemia during deep hypothermic circulatory arrest (DHCA) have been held responsible, but brain injury is increasingly recognised as multi-factorial.  Of particular importance are the systemic inflammatory response and period of reperfusion, both of which contribute exigently to the progression of injury.  The aims of this project were to identify techniques whereby the inflammatory and post-ischaemic reperfusion components can be harnessed to modulate the response to DHCA.

In a series of neonatal piglet experiments, strategies for reducing the systemic inflammatory load, methods for protecting against ischaemia through induction of tolerance and identifying facets of the reperfusion period that exacerbate injury have been examined.  Furthermore, using a novel technique of contrast magnetic imaging, preliminary studies have been performed aimed at identifying and quantifying the ultrastructural injury resulting from neonatal perfusion techniques.

The results have indicated that: 1) Avoiding allogeneic blood se in neonatal CPB leads to significantly reduced systemic and cerebral inflammation, and that cerebral no-reflow can be avoided; 2) Hypoxaemic reperfusion in cyanotic congenital repair exacerbates the neurological injury sustained during DHCA; 3) Delayed preconditioning through lipopolysaccharide administration can confer robust neurological protection against ischaemia during DHCA; and 4) Gadolinium MRI may be a useful tool for the quantification of blood-brain barrier injury following CPB and allow further characterisation of the cerebral impact of CPB strategies.

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