Neurological damage due to coagulation and fat release during cardiopulmonary bypass

Cardiac surgery with cardiopulmonary bypass (CPB) has been associated with a higher risk of neurologic and neuropsychological deficits than other major types of surgery [ 1 ]. Different etiologic mechanisms have been proposed to account for these deficits [ 2 , 3 , 4 , 5 ]. First, inadequate perfusion of the brain circulation has been proposed as a factor of brain damage. Second, CPB produces a systemic inflammatory response that may give rise to renal and pulmonary dysfunction, but the effect on the brain has attracted less attention [ 6 , 7 ]. Although a causal relationship has been suggested between the inflammatory response and cognitive dysfunction [ 8 ], no clear evidence exists. Third, emboli are formed during CPB by air, clotting activity or cell aggregation and fat release. Partly, these emboli are captured by the various filters in the circuit, but reorganization of smaller emboli might still occur. By comparing several studies in which markers for brain damage were used, these three major mechanisms are discussed.