Delayed paraplegia after thoracoabdominal aortic aneurysm repair announced by changes in CSF

Abstract

Delayed paraplegia is an unpredictible, albeit devastating complication of thoracoabdominal aortic aneurysm (TAAA) repair [1]. We report on a patient who, 24 hours after TAAA repair, developed paraplegia that was announced by biochemical changes in cerebrospinal fluid (CSF). A 57-year-old man was submitted to TAAA repair. A lumbar spinal drain was placed after induction of anesthesia and left in place in order to reduce CSF pressure and sample collection. Samples were collected immediately after catheter placement and at time intervals during aortic cross-clamping, after cross-clamp release and postoperatively in the ICU, and stored at -80°C. Excitatory and inhibitory amino acids (glutamate, aspartate, glycine, GABA), non-transmitter amino acids (taurine, alanine), energetic metabolism parameters (lactate, adenosine) were analyzed by HPLC altogether 5 days later. The surgical procedure was performed with the aid of a left-side bypass. Fifteen minutes after proximal aortic cross-clamping, excitatory, inhibitory and nontransmitter amino acids in the CSF increased several times with respect to baseline and stayed high throughout reperfusion. Proximal aortic cross-clamping resulted also in an increase of lactate that stayed high also during reperfusion, while adenosine, a product of purine metabolism, increased during cross-clamping and normalized at reperfusion. Four hours after the end of surgery, while the patient was in the ICU, all parameters returned to baseline. The following day, a new sample of CSF was collected. At that time the patient was awake, hemodynamically stable, CSF pressure was 10 mmHg, and his lower extremities motility was preserved. Three hours later he developed paraplegia. Emergency CT scan excluded epidural hematoma. The analysis of the CSF sample collected 3 hours prior to the onset of paraplegia showed an increase of excitatory, inhibitory and nontransmitter amino acids, as well of lactate and adenosine. Altogether our findings indicate that the biochemical changes that occurred in the CSF of our patient announced the impending spinal cord ischemia. Bedside, real-time evaluation of the biochemical changes in CSF, which has been recently made possible by new apparatus, could be useful to evaluate spinal cord perfusion and, hopefully, to contrast the onset of paraplegia associated with TAAA repair.