We thank Harrison et al. for their comments and interest in our recent article. 1We appreciate that they considered important our observation that surface hypothermia to a core temperature of 32°C did not depress median nerve somatosensory evoked potentials (SSEP) amplitude but rather prolonged latency. We also agree that this has implications for patients undergoing certain orthopedic and vascular surgical procedures in which SSEPs are monitored.
Harrison et al. remarked that we did not state the mean total duration of induced hypothermia. Note that duration of hypothermia with an esophageal temperature of approximately 32°C depended on surgical resection time, which, of course, varied between individuals. However, total duration of marked hypothermia of 32°C, as required for resection of choroidal melanoma, averaged 101 min ± 40 (SD). Thus, there was ample time for temperature equilibration across the body, including the spinal cord.
We agree that it would be interesting to know precisely how rapidly spinal cord and esophageal temperatures equilibrate in patients undergoing certain surgical procedures during hypothermia, and to exactly what degree spinal cord temperature influences SSEPs. Obviously, however, intraspinal cord temperature measurements with a thermistor-tipped pulmonary artery catheter, as suggested by Harrison et al. , are hardly feasible in humans undergoing eye surgery. However, as reported by Kumar et al. , there is a close correlation between intrathecal and core temperatures (r = 0.873; P < 0.001) during proximal aortic surgery, 2and during aortic clamping, intrathecal temperature is close to intraaortic temperature in rats. 3
Thus, esophageal temperature during hypothermia, when maintained for some time, is likely similar to intrathecal temperature. Regardless, our data show that surface hypothermia to an esophageal temperature of 32°C does not depress median nerve somatosensory evoked potentials amplitude but rather prolongs their latency.
