Alterations to haemostasis following cardiopulmonary bypass and the relationship of these changes to neurocognitive morbidity.

Cardiopulmonary bypass (CPB) is routinely utilized to provide circulatory support during cardiac surgical procedures. The morbidity of CPB has been significantly reduced since its introduction 50 years ago; however, cerebral injury remains a potentially serious consequence of otherwise successful surgery. The risk of stroke postoperatively is approximately 1-5%. Incidence rates for neurocognitive deficit, however, vary markedly depending on the detection method, although typically it is reported in at least 50% of patients. The aetiology of this cerebral injury remains open to debate, although evidence shows that ischaemia secondary to microembolism may be the principal factor. Emboli originate from bubbles of air, atheroemboli released on aortic manipulation and thromboemboli generated as a result of haemostatic activation. Significant generation of thrombin occurs during CPB resulting in fibrin formation, although the trigger of this activation is not fully understood. Rather than originating from contact activation as previously thought, the primary trigger may be via the activated factor VII/tissue factor pathway of coagulation, with an additional role of contact activation in amplification of coagulation as well as the fibrinolytic response to CPB. Haemostatic activation is inhibited with systemic heparin therapy. The relationship between haemostatic activation and emboli formation during CPB is not known. Interventions to reduce cerebral injury in the context of cardiac surgery depend, in large part, on the minimization of emboli. This review investigates cerebral injury after cardiac surgery and evidence showing that microembolism is the principal causative agent. Fibrin emboli are postulated to be an important source of cerebral embolism. The mechanism of haemostatic activation during CPB is therefore also discussed.