S J Mitchell1, O Pellett, D F Gorman. 1. Royal New Zealand Navy Hospital, Cardiothoracic Surgical Unit, Auckland, New Zealand.
Abstract
BACKGROUND:Lidocaine improves outcome in animal brain injury models. Cardiac operations often cause postoperative neuropsychological (NP) impairment. We investigated cerebral protection by lidocaine in cardiac surgical patients. METHODS:Sixty-five patients undergoing left heart valve procedures completed 11 preoperative NP tests, a self-rating inventory for memory, and inventories measuring depression and anxiety. These were repeated 10 days, 10 weeks, and 6 months postoperatively. Patients received a 48-hour double-blinded infusion of either lidocaine in a standard antiarrhythmic dose or placebo, beginning at induction of anesthesia. A postoperative deficit in any test was defined as decline by more than or equal to the group preoperative standard deviation. In addition, sequential postoperative percentage change scores were calculated for each patient in all NP tests and the inventories for memory, depression and anxiety. RESULTS:Forty-two patients completed all three reviews, 8 completed two reviews, and 5 patients were reviewed once. Significantly more placebo patients had a deficit in at least one NP test at 10 days (p<0.025) and 10 weeks (p<0.05). The lidocaine group achieved superior sequential percentage change scores in 6 of the 11 NP tests (p<0.05) and in the memory inventory (p<0.025). There were no group differences in the remaining NP tests or the depression and anxiety inventories. CONCLUSIONS: These data show that cerebral protection by lidocaine, which is unrelated to any effect on depression or anxiety, and is at a level that is noticed by the patients.
RCT Entities:
BACKGROUND:Lidocaine improves outcome in animal brain injury models. Cardiac operations often cause postoperative neuropsychological (NP) impairment. We investigated cerebral protection by lidocaine in cardiac surgical patients. METHODS: Sixty-five patients undergoing left heart valve procedures completed 11 preoperative NP tests, a self-rating inventory for memory, and inventories measuring depression and anxiety. These were repeated 10 days, 10 weeks, and 6 months postoperatively. Patients received a 48-hour double-blinded infusion of either lidocaine in a standard antiarrhythmic dose or placebo, beginning at induction of anesthesia. A postoperative deficit in any test was defined as decline by more than or equal to the group preoperative standard deviation. In addition, sequential postoperative percentage change scores were calculated for each patient in all NP tests and the inventories for memory, depression and anxiety. RESULTS: Forty-two patients completed all three reviews, 8 completed two reviews, and 5 patients were reviewed once. Significantly more placebo patients had a deficit in at least one NP test at 10 days (p<0.025) and 10 weeks (p<0.05). The lidocaine group achieved superior sequential percentage change scores in 6 of the 11 NP tests (p<0.05) and in the memory inventory (p<0.025). There were no group differences in the remaining NP tests or the depression and anxiety inventories. CONCLUSIONS: These data show that cerebral protection by lidocaine, which is unrelated to any effect on depression or anxiety, and is at a level that is noticed by the patients.