T Hirotani1, T Kameda, T Kumamoto, S Shirota. 1. Department of Cardiovascular Surgery, Tokyo Saiseikai Central Hospital, 1-7-14 Mita, Minato-ku, 108-0073, Tokyo, Japan. hero.takashi@nifty.ne.jp
Abstract
OBJECTIVE: Hypothermic circulatory arrest is a standard procedure for the treatment of aortic arch. However, there is a time limit for this procedure. There is now an urgent need to develop prophylactic measures to extend the time limit. We have used a pharmacological mixture of thiopental, nicardipine and mannitol for all patients undergoing circulatory arrest since 1991 to extend the safe limit. The purpose of this study was to analyze the neurological complications demonstrated by these patients and to evaluate the brain-protective effects of our measure. METHODS: The clinical records of 75 consecutive patients undergoing an aortic arch repair using a hypothermic circulatory arrest technique during the past 8 years were retrospectively reviewed. Systemic cooling was continued until a total disappearance of EEG activity. Prior to circulatory arrest, 15 or 30 mg/kg of thiopental, 20 mg of nicardipine and 300 ml of mannitol were infused into the venous reservoir of a cardiopulmonary bypass circuit. Graft replacement was performed in all patients and the extent of replacement was a total aortic arch in 43 patients, a distal aortic arch in 17, a hemiarch in 13 and a distal aortic arch and a total descending aorta in two. RESULTS: The duration of circulatory arrest ranged from 16 to 80 min (mean 41.5 min), and it exceeded 45 min in 37 patients. Operative mortality was 10.7% and two patients died of stroke. Three patients had permanent and three other patients had transient neural deficits. The incidence of stroke was 8.0% as a whole, and no correlation between the incidence of neurological complications and the duration of circulatory arrest was found. A multivariate analysis showed that the duration of circulatory arrest was determined as a predictor of neither operative mortality nor postoperative stroke. CONCLUSIONS: The findings of the present study suggest that our pharmacological brain protection appears to be effective for safely extending hypothermic circulatory arrest.
OBJECTIVE:Hypothermic circulatory arrest is a standard procedure for the treatment of aortic arch. However, there is a time limit for this procedure. There is now an urgent need to develop prophylactic measures to extend the time limit. We have used a pharmacological mixture of thiopental, nicardipine and mannitol for all patients undergoing circulatory arrest since 1991 to extend the safe limit. The purpose of this study was to analyze the neurological complications demonstrated by these patients and to evaluate the brain-protective effects of our measure. METHODS: The clinical records of 75 consecutive patients undergoing an aortic arch repair using a hypothermic circulatory arrest technique during the past 8 years were retrospectively reviewed. Systemic cooling was continued until a total disappearance of EEG activity. Prior to circulatory arrest, 15 or 30 mg/kg of thiopental, 20 mg of nicardipine and 300 ml of mannitol were infused into the venous reservoir of a cardiopulmonary bypass circuit. Graft replacement was performed in all patients and the extent of replacement was a total aortic arch in 43 patients, a distal aortic arch in 17, a hemiarch in 13 and a distal aortic arch and a total descending aorta in two. RESULTS: The duration of circulatory arrest ranged from 16 to 80 min (mean 41.5 min), and it exceeded 45 min in 37 patients. Operative mortality was 10.7% and two patients died of stroke. Three patients had permanent and three other patients had transient neural deficits. The incidence of stroke was 8.0% as a whole, and no correlation between the incidence of neurological complications and the duration of circulatory arrest was found. A multivariate analysis showed that the duration of circulatory arrest was determined as a predictor of neither operative mortality nor postoperative stroke. CONCLUSIONS: The findings of the present study suggest that our pharmacological brain protection appears to be effective for safely extending hypothermic circulatory arrest.