Neuropathological Findings in Patients Dying after Open-heart Surgery

Hypotension-Induced Changes in Cerebral Function During Cardiac Surgery

“…The neuropathological lesions in Cases 1 and 2 of this series were similar to those found by Brierley and coworkers 6 -'• 32~34 and Gilman 8 in humans following intraoperative hypotensive episodes. Similar findings of diffuse, bilateral involvement of cerebral and/or cerebellar cortices with accentuation in arterial boundary zones were observed by Brierley et al 35 in later studies of experimental hypotension in the rhesus monkey.…”

“…4 -5 Other investigators who correlated histological evidence of ischemic anoxia following CPB with extracorporeal perfusion pressure have suggested that hypotension during CPB may also contribute to CNS dysfunction following cardiac surgery. 6 " 10 However, in none of these studies was the intraoperative blood pressure recorded continuously and, in the only one in which the EEG was monitored during bypass, 9 the EEG findings were not discussed. Thus, there was no direct evidence that low perfusion pressures were responsible for the ischemia which produced the lesions in these studies.…”

Brain damage and neurological outcome after open-heart surgery.

“…In this study, the preoperative signs and case histories referred to the left hemis.phere in 70% of cases but, by contrast, the postoperative signs originated from the right hemisphere in 71 %. Hemiparesis, which was the most usual major complication, was left-sided in 16 of the 22 cases in which the origin could be localised to the cerebral level. These cases were analysed with special care in relation to preoperative, intraoperative, and postoperative variables but no explanation could be stated on clinical grounds to the disparity between right and left hemispheral involvement.…”

Spontaneous Cerebellar Hemorrhage after Coronary Artery Bypass Surgery

“…Cerebral complications have been at tributed to macroembolization of air or par ticulate matter, microembolization of air, fat, platelet-fibrin aggregates, foreign particles or antifoaming agents. Other causes of brain damage relate to inadequate cerebral perfu sion in patients predisposed by prior cerebro vascular disease, prolonged cardiopulmonary bypass, or low perfusion pressures due to inadequate capillary bed perfusion [1][2][3][4][5][6][7][8][9][10][11][12]. The pathologic entities usually described in clude focal or multifocal infarcts, emboli lodged in small cerebral vessels, cerebral edema and intracranial hemorrhage [5][6][7], usually petechial, pcrvascular or focal in the subarachnoid space.…”