Purine nucleoside use as surrogate markers of cerebral ischaemia during local and general anaesthetic carotid endarterectomy.

OBJECTIVES: In periods of cerebral ischaemia, adenosine triphosphate is metabolised, leading to accumulation of adenosine inosine and hypoxanthine. These can be measured in real time using peripheral blood samples intraoperatively. The primary aim of this study was to describe changes in purine concentrations in a cohort of patients undergoing carotid endarterectomy under general anaesthetic, and to evaluate correlation between changes in values with major perioperative steps. The secondary aim was to compare changes in concentrations with a previous cohort of patients who had undergone carotid endarterectomy under local anaesthetic. METHODS: This was a prospective observational study. Purine concentrations were determined from arterial line samples and measured via an amperometric biosensor at specific time points during carotid endarterectomy. Mean arterial pressure was manipulated to maintain steady cerebral perfusion pressure throughout the procedure. These results were analysed against data from a cohort of patients who underwent carotid endarterectomy under local anaesthetic in previously published work. RESULTS: Valid results were obtained for 37 patients. Purine concentrations at baseline were 3.02 ± 1.11 µM and 3.16 ± 1.85 µM for the unshunted and shunted cohorts, respectively. There was no significant change after 30 min of carotid clamping at 2.07 ± 0.89 and 2.4 ± 3.09 µM, respectively (both p > 0.05). Peak purine during the clamp phase in the loco-regional anaesthetic cohort was 6.70 ± 3.4 µM, which was significantly raised compared to both general anaesthetic cohorts (p = 0.004). There were no perioperative neurological events in either cohort. CONCLUSION: This small study does not demonstrate conclusive evidence that purine nucleosides can be used as a marker of cerebral ischaemia; the comparisons to the loco-regional anaesthetic data offer information about differences in the cerebral adenosine triphosphate metabolism between general anaesthetic and loco-regional anaesthetic. We hypothesise that the lack of a rise in purine nucleosides under general anaesthetic may be caused by a decrease in the cerebral metabolic rate and loss of metabolic rate-blood flow coupling caused by general anaesthetic agents.