Similar to other methods of organ preservation, "spinoplegia" may protect the spinal cord from the effects of oxygen desaturation during aortic cross-clamping. In porcine experiments, spinal cord O2 saturation was studied during introperative localization of the blood supply to the spinal cord using hydrogen; division of arteries not supplying the spinal cord; aortic cross-clamping for 60 minutes; and 60 minutes after unclamping. In 5 animals, 120 mL of cold saline solution with lidocaine (100 mg/dL) was infused into the aorta during aortic cross-clamping. During sequential localization, O2 saturation dropped by 40.02% (standard deviation, 20.16%) for T-14 artery testing versus a decrease of 17.27% (standard deviation, 11.88%; p = 0.0075) for L-5 artery segment testing in the control animals and returned to baseline thereafter. During arotic cross-clamping maximal O2 desaturation was 5% of baseline (15.7%; p < 0.0001), which improved slightly by 30 minutes after clamping (48% of baseline +/- 37.37%; p = 0.048 versus maximum) and then returned to baseline (97.1% of baseline +/- 41%) with unclamping; 5 minutes later, hyperoxygenation occurred with a progressive decline thereafter (68% of baseline +/- 29.3%; p = 0.025, 45 minutes after unclamping versus baseline). The decrease in spinal motor evoked potentials was significantly less (p < 0.02) in the treated group. Intraoperative hydrogen testing in 8 patients was demonstrated to be safe. It accurately localized reattached arteries, and O2 saturation of the spinal cord fell by 56% (standard deviation, 29%; p = 0.0025) with aortic cross-clamping. We conclude that spinal cord ischemia occurs with aortic cross-clamping in both animals and humans. Preservation of hydrogen-localized arteries maintains oxygenation of the spinal cord and is accurate in both animals and humans. Segmental infusion of a "spinoplegia" prevented the loss of spinal motor evoked potentials. Further research may identify improved spinal cord preservation techniques, including "spinoplegia," and effective agents.

Permanent ligation of arteries supplying blood to the spinal cord in operations for aortic aneurysm can lead to spinal cord ischemia, which can result in either paraparesis or paraplegia. This report describes a rapid method of intraoperative identification of those arteries that supply the spinal cord by use of an intrathecal platinum electrode to detect hydrogen in solution that has been injected into the aortic ostia. Preservation or perfusion of those identified arteries supplying the spinal cord may decrease the rate of postoperative neurologic complications. Of 28 porcine experiments with postoperative observation for 24 hours, there were 3 initial pilot experiments in which saline saturated with hydrogen was injected into the temporarily cross-clamped aorta. Twenty animals were then randomized to (1) preservation of only the vessels sequentially identified to supply blood to the spinal cord from T-13 to L-5 (n = 10); (2) division of the vessels supplying the spinal cord (n = 10). A further five animals underwent perfusion experiments wherein the identified cord arteries were perfused by a shunt, the other nonsupply arteries were divided, and the aorta was kept clamped for 45 minutes. Spinal motor evoked potentials were elicited with an intrathecal electrode and were highly sensitive for paralysis. Paralysis occurred in 0/3 pilot (p less than 0.013 vs division); 8/10 division; 1/10 preservation (p less than 0.0017 vs division); and perfusion 1/5 (p less than 0.025 vs division). Results of a pilot study in eight humans shows that the technique can be used to rapidly identify segmental arteries supplying the spinal cord, to determine if distal perfusion is supplying the spinal cord with blood flow, and if reattached segmental arteries are patent.

One source of paraplegia after aortic operations is the failure to reattach the spinal cord blood supply, the origins of which are not evident at operation. This report is concerned with a rapid new method of identifying these vessels intraoperatively. In 9 pigs, a specially designed catheter with platinum and stainless steel electrodes was inserted intrathecally. Saline solution saturated with hydrogen was injected sequentially into arterial ostia at T-15 to L-4 inclusive, and the generated current impulses from the conditioned platinum electrode were recorded. Of 90 potential segmental arteries supplying the spinal cord, 28 gave rise to spinal radicular arteries. Hydrogen-induced current impulses correctly located 25 of the radicular arteries and all those larger than 180 microns in diameter. When injected with indigo carmine, the vessels localized by the hydrogen-induced current impulses filled the entire anterior spinal artery from the low thoracic to the sacral region, whereas injection of the other vessels did not show filling. After refinement and testing for safety, this method has been employed clinically to rapidly localize and reattach routes of critical cord circulation.

Profound hypothermia protects cerebral function during circulatory arrest in the surgical treatment of a variety of cardiac and aortic abnormalities. Despite its importance, techniques to determine the appropriate level of hypothermia vary; studies of temperatures recorded from multiple peripheral body sites show inconsistent findings. The purpose of this study is to establish objective criteria to consistently identify intraoperatively the safe level of hypothermia. Our studies are based on experimental evidence showing a correlation between brain temperature and development of electrocerebral silence (ECS) on the electroencephalogram (EEG), and the recognition that the EEG, as an objective measure of brain function, can easily be recorded intraoperatively. We studied 56 patients who required circulatory arrest during operation for replacement of the ascending aorta or aortic arch (N = 55) or aortic valve replacement (N = 1). Peripheral body temperatures from the nasopharynx, esophagus, and rectum and the EEG were continuously recorded during body cooling. Circulatory arrest time ranged from 14 to 109 minutes. No peripheral body temperature from a single site or from a combination of sites consistently predicted ECS. There was a wide variation in temperature among body sites when ECS occurred: nasopharyngeal, 10.1° to 24.1°C; esophageal, 7.2° to 23.1°C; rectal, 12.8° to 28.6°C. Fifty-one (91%) of the 56 patients survived. Three had neurological deficits, none clearly related to hypothermia. Two patients (3.6%) required reexploration for postoperative bleeding. We conclude that monitoring the EEG to identify ECS is a safe, consistent, and objective method of determining the appropriate level of hypothermia.