Munir Boodhwani, Fraser D. Rubens, Denise Wozny, Rosendo Rodriguez, Howard J. Nathan; Cardiac Surgery, University of Ottawa Heart Institute, Ottawa, ON, Canada
Objective: Neurocognitive dysfunction occurs frequently following cardiac surgery. While cerebral hypothermia has been proposed as a neuroprotective strategy, recent evidence based guidelines reveal a lack of consensus regarding optimal temperature management in cardiac surgical patients. We have previously reported poorer neurologic outcome in patients who underwent rewarming (32°C to 37°C) compared to no rewarming (32°C to 34°C). We sought to validate these observations and evaluate the effects of sustained mild intra-operative hypothermia, without rewarming, on neurocognitive function following coronary artery bypass surgery (CABG).Methods: Patients (age>60 years) undergoing non-emergent CABG were randomized to intra-operative nasopharyngeal temperature of 34°C (hypothermic; n = 133) or 37°C (normothermic; n = 134) maintained, during the entire intra-operative period, using water-circulating thermal control pads. No active rewarming was employed. Transcranial Doppler was used to monitor middle cerebral artery emboli. Neuropsychometric testing (battery of 16 tests) was performed by blinded observers pre-operatively, prior to discharge, and at 3 months, and tests were divided into four cognitive domains. A post-operative cognitive deficit (POCD) was prospectively defined as a one standard deviation drop in individual scores from baseline in = 1 domain. Quality of life (QOL) was evaluated at 3 months.
Results: The number of intra-operative cerebral emboli was similar between normothermic and hypothermic groups (188 [115-331] vs. 182 [100-305], p = 0.71). At discharge, POCDs were present in 45% of normothermic and 49% of hypothermic patients (p = 0.49) and at 3 months, decreased to 8% in normothermic and 4% in hypothermic patients (p = 0.28). There was no correlation between cerebral emboli and the occurrence of POCDs (r = -0.01; p = 0.88). Hypothermic patients demonstrated trends towards shorter intensive care unit stay (1.4 ± 1.0 vs. 1.2 ± 0.7 days, p = 0.06) and increased chest tube output (655 ± 327 vs. 584 ± 325 ml/12 hours, p = 0.09) with no difference in transfusion rates (p = 0.14). Patients with POCDs reported a greater decline in the mental component of QOL at 3 months (p=0.004).
Conclusion: Mild intra-operative hypothermia is safe but, in the absence of rewarming and cerebral hyperthermia, does not improve neurocognitive outcome in patients undergoing CABG. Intra-operative cerebral emboli are not predictive of POCDs. These results argue against an ischemic, embolic etiology for POCDs.
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