Dextrose administration increases sensory/motor impairment and paraplegia after infrarenal aortic occlusion in the...

Spinal ischemia with resultant cord infarction is a catastrophic complication of surgical procedures involving the thoracoabdominal aorta. A rabbit spinal ischemia model was used to test if glucose administration would increase neurologic deficit of the lower extremity. Rabbits (2 to 3 kg), anesthesized with halothane, had a snare occluder placed around the aorta just below the left renal artery. After a 2-hour recovery, the aorta was occluded for 15 minutes. Before occlusion animals received an intraperitoneal injection of isotonic glucose (2 gm/kg; n = 11), isotonic mannitol (2 gm/kg; n = 3), or an equal volume of saline solution (n = 11). Four sham-operated animals received glucose and an identical surgical procedure, but the aorta was not occluded. Average blood glucose level at the time of occlusion for the glucose group was 249 +/- 15 versus 156 +/- 6 for the control group (p less than 0.01). At 1, 4, 18, and 24 hours, a neurologic impairment score (1 = normal, 2 = partial impairment, 3 = complete impairment) was assigned. At 4, 18, and 24 hours, the glucose group had significantly greater neurologic impairment than did control groups (p less than 0.02). Glucose administration had an adverse effect in a controlled and highly reproducible model of spinal cord ischemia. Exogenous glucose administration should potentially be avoided during complex aortic reconstruction.