CLINICAL MARKERS IN CSF FOR DETERMINING NEUROLOGIC DEFICITS AFTER THORACOABDOMINAL AORTIC-ANEURYSM REPAIRS

Background. Spinal cord ischemia is a major cause of morbidity and mor tality after thoracoabdominal, aortic aneurysm operations. The inciden ce of paraplegia is high even in experienced institutions. Methods. We investigated whether neurotransmitter excitotoxicity is associated wi th neurologic deficits after thoracoabdominal aortic aneurysm operatio ns. We hypothesized that patients with spinal cord injury would manife st elevated levels of excitatory amino acids in their cerebrospinal fl uid. Sixteen patients undergoing thoracoabdominal aortic aneurysm oper ations had cerebrospinal fluid drawn through lumbar spinal drains preo peratively, intraoperatively, and postoperatively. Excitatory amino ac id levels (glutamate, aspartate, glycine) were measured using high-per formance liquid chromatography. Excitatory amino acid levels were comp ared in patients who exhibited no neurologic deficits postoperatively (group I; n = 12) with patients who had clinically evident lower extre mity and cerebral neurologic deficits (group II; n = 4). Results. Sign ificant elevations in glutamate and aspartate levels from baseline (p < 0.05) were limited to group II. Excitatory amino acid levels in grou p II were significantly elevated (p < 0.05) compared with those observ ed in group I. Glutamate levels were especially increased during aorti c cross-clamping and late reperfusion, whereas aspartate levels were i ncreased only during late reperfusion. Conclusions. These data suggest that neurotransmitter excitotoxicity plays a significant role in cent ral nervous system injury. (C) 1997 by The Society of Thoracic Surgeon s.