Nevin, Michael; (1990) The role of per-operative monitoring in the prevention of neurological deficit following coronary artery bypass surgery. Doctoral thesis (M.D), UCL (University College London).

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Abstract

Post-operative neuropsychometric deficit is now a well accepted complication of coronary artery bypass surgery. Little is known of the aetiology of this deficit , although both cerebral hypoperfusion and cerebral microembolisation have been cited as likely causes, despite a lack of hard confirmatory evidence. This study sets out, by means of intensive monitoring to investigate per-operative factors that may be contributing to this deficit and to identify areas requiring future improvement. 65 patients undergoing isolated coronary artery surgery and 15 patients undergoing peripheral vascular surgery underwent detailed neuropsychometric and ophthalmological assessments pre-operatively and again twice in the first post-operative week. Per-operatively arterial and jugular bulb venous pressures, arterio-venous (jugular) oxygen content differences and blood gas tensions were monitored frequently but the surgeon and anaesthetist were not informed of the results. In 35 patients (Group A), ventilatory perameters were at the discretion of the anaesthetist, who referred to his own intermittent blood gas samples according to accepted practice. In the remaining 30 cardiac patients (Group B), end-tidal CO2 monitoring was utilised pre-bypass and an arterial "in-line" CO2 electrode per-bypass, to maintain a state of normocapnia throughout the operation. The patients were otherwise subjected to identical surgical and anaesthetic protocol as Group A. 15 patients undergoing peripheral vascular surgery (Group C) were subjected to a similar per-operative management as Group A with ventilatory parameters at the discretion of the anaesthetist. Post-operatively a significant neuropsychometric deficit was detected in 71% of Group A patients but only 4 0% of Group B. and 27% of Group C. Ophthalmological changes, consistent with ocular hypoperfusion, were found in 20% of Group A. Neither Groups B nor C demonstrated any evidence of new ophthalmological signs post-operatively. Statistical analysis of the data from the two cardiac groups revealed that Group A members demonstrated a significantly greater incidence of post-operative neurological deficit associated with; 1. lower mean PaCO2 value, and a higher mean cerebral arterio-venous oxygen content difference immediately prior to the onset of perfusion. 2. significantly greater increases in cerebral venous pressure (consequent upon excessive fluctuations in measured CO2 tensions), following the onset of the perfusion period. 3. significantly lower cerebral perfusion pressures in the first ten minutes following the onset of bypass; a period not maximally covered by the protective benefits of hypothermia. Examination of the results from the non-cardiac patients (Group C) showed a strong correlation between a combination of mean per-operative PaCO2 values / per-operative blood loss and the incidence of post-operative deficit. Group A and Group C results suggest that inadequate per-operative monitoring often results in extreme degrees of unrecognised hypocapnia; while crude attempts at correcting this can often compound the problem by inducing a hypercapnic state in which cerebral autoregulation is lost. Group B showed a significant reduction in post-operative deficit as a result of "on-line" manipulation of per-operative parameters.

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