CHOREOATHETOSIS AFTER DEEP HYPOTHERMIA WITHOUT CIRCULATORY ARREST

In 8 of 758 patients undergoing an intracardiac operation under cardiopulmonary bypass and hypothermia, choreoathetosis developed 3 to 7 days postoperatively. Before the onset of choreoathetosis, varying degrees of neurological dysfunction were noted. Electroencephalography and neuroimaging failed to detect any responsible functional or structural changes. Six patients are alive 1 to 3 years postoperatively, and their condition is improving. Two patients died of aspiration or sepsis. All patients were grouped based on factors identified as being possibly causative: depth of hypothermia, cooling time, flow rate, and repeated hypothermia. The incidence of choreoathetosis was significantly different in group A (rectal temperature > 25 °C compared with group B (rectal temperature ≤ 25 °C) ( 0 295 versus 8 463; p = 0.02). Based on cooling time, the incidence of choreoathetosis was significantly different in group B1 (cooling time < 1 hour) compared with group B2 (cooling time ≥ 1 hour) ( 1 220 versus 7 243; p = 0.05). Based on flow rate during cooling, group B2 was further divided into the low-flow group (< 1,500 mL · min-1 · m-2) and the high-flow group (≥ 1,500 mL · min-1 · m-2). Although not significant, the incidence of choreoathetosis was higher in the high-flow group ( 6 153) versus 1 90; p = 0.22). In group B patients having reoperation, the incidence of choreoathetosis was higher than in patients operated on for the first time (5/54 versus 3 409; p <- 0.0001). Our data suggest that deep hypothermia of 25 °C or lower along with a cooling time of 1 hour or longer, maintenance of a high flow rate, and repeated exposure to hypothermia may predispose to the development of choreoathetosis postoperatively. © 1990.