• R A Boyajian, D F Sobel, G A DeLaria, and S M Otis.
• Division of Neurology, Scripps Clinic and Research Foundation, La Jolla, CA 92037, USA.
• J Neuroimaging. 1993 Jan 1; 3 (1): 1-5.

AbstractTha pathophysiology of brain injury in patients undergoing cardiopulmonary bypass remains unclear despite several decades of inquiry. The advent of noninvasive high-resolution brain and cerebrovascular imaging by magnetic resonance, computed tomography, and pulsed Doppler ultrasonography now permits in vivo assessment of pathophysiological mechanisms. Neuroradiographic and carotid duplex studies were performed in patients who developed neurological deficits following cardiopulmonary bypass. Among 30 symptomatic patients undergoing magnetic resonance or computed tomography brain scans, 18 (60%) had findings of acute ischemic injury. Embolic infarction was evident in 14 (78%) of these 18 patients. Watershed injury was the predominant finding in a single patient, while findings consistent with global anoxia were present in another patient. Carotid atheroemboli were excluded as a possible source of embolism in 11 patients whose carotid duplex studies were unremarkable preoperatively as well as in 3 further patients whose neuroradiographic findings did not correspond with their moderate carotid disease. It is concluded that infarction due to noncarotid embolism is the primary pathophysiology of neurological deterioration following cardiopulmonary bypass.

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