Cerebrospinal fluid markers of brain injury, inflammation, and blood-brain barrier dysfunction in cardiac surgery.

Background Neurocognitive dysfunction occurs frequently after open-heart surgery. Cerebral microembolization, inflammation, blood-brain barrier (BBB) dysfunction, and impaired cerebral oxygenation are considered among possible etiologies. The relationships between intraoperative microembolic signals and the release of cerebrospinal fluid (CSF) markers of inflammation, neuronal and glial cell injuries, and BBB function were evaluated after cardiac surgery with cardiopulmonary bypass. Methods Ten patients undergoing aortic valve replacement were included. The CSF was obtained the day before and 24 hours after surgery for assessment of neuronal damage (neuron-specific enolase, total tau, and neurofilament light chain protein), glial cell injury (S-100B, glial fibrillary acidic protein), BBB integrity (CSF to serum albumin ratio) and cytokines (interleukin-6, interleukin-8). Intraoperative extent of microemboli and their occurrence were described using the transcranial Doppler technique. Results Intraoperatively, 354 ± 79 microemboli were detected; 81% after release of the aortic cross clamp. The S-100B and glial fibrillary acidic protein increased by 35% ( p p = 0.055), respectively. Neuron-specific enolase, total tau, and neurofilament light chain protein, were not significantly affected by the surgery. The CSF albumin increased by 13% ( p p p = 0.011). There was a 3.5- and 12-fold increase in interleukin-6 ( p p Conclusions Cardiac surgery with cardiopulmonary bypass causes cerebral inflammation, glial cell injury, and BBB dysfunction without biochemical signs of neuronal damage. These changes are not associated with intraoperative microembolization.