Introduction: Cardiopulmonary bypass (CEC) in the surgical treatment of cardiac diseases may cause the appearance of neurological damage of an intensity which varies between minor neuropsychological disorders and global cerebral anoxia. There are two mechanisms for the production of these lesions: ischaemic and embolic. The mortality associated with this type of complication is low, but morbidity may be considerable. The neurological disorders derived from CEC may be classified according to the aetiology and clinical findings. In the first group are included: severe cerebral anoxia, embolic cerebro-vascular accidents, microvascular embolias, lesions of spinal vascularization and lesions of the peripheral nerves. In the second group are: encephalic focal lesions, convulsive crises, lesions of the extra-pyramidal system, alterations in the level of consciousness and neuropsychological disorders.
Methods: Quantification of neuronal damage has been attempted by: monitoring cerebral blood flow and neurone metabolism, EEG and study of intra-operative evoked potentials, echography of the carotid, cardiac and ascending aorta, transcranial doppler, fluorescein-angiography and the study of biochemical markers of neuronal and glial damage. Different studies have identified a series of factors which potentiate the risk of neurological lesions following CEC. These are: age, severe carotid disease, aortic atherosclerosis and previous cerebro-vascular haemorrhage, amongst others. An attempt is made to reduce the incidence of neurological complications by: pre-operative evaluation of carotid bruits, hypothermia, careful surgical technique and the use of drugs with a neuroglial protector effect. None of these methods gives sufficiently effective protection to the central nervous system subjected to the changes involved in the use of CEC.
Conclusion: There are still many unknown aspects of neurone pathology in these circumstances, leaving a door open to investigation.