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J Thorac Cardiovasc Surg 2003;126:1288-1294
© 2003 The American Association for Thoracic Surgery

Surgery for acquired cardiovascular disease

Preoperative and operative predictors of delayed neurologic deficit following repair of thoracoabdominal aortic aneurysm

^a Department of Cardiothoracic and Vascular Surgery, Memorial Hermann Hospital, Houston, Tex, USA
^b The University of Texas at Houston Medical School, Memorial Hermann Hospital, Houston, Tex, USA

Read at the Eighty-second Annual Meeting of The American Association for Thoracic Surgery, Washington, DC, May 5-8, 2002.

Received for publication May 14, 2002; revisions received July 8, 2002; revisions received April 24, 2003; accepted for publication June 3, 2003.

^* Address for reprints: Hazim J. Safi, MD, The University of Texas at Houston Medical School, Department of Cardiothoracic and Vascular Surgery, UTH Medical Center, Suite 450, 6410 Fannin Street, Houston, TX 77030, USA
Hazim.J.Safi{at}uth.tmc.edu

PURPOSE: Delayed neurologic deficit has been recognized in recent years as a source of morbidity following thoracic and thoracoabdominal aortic repair. We wanted to find risk factors specifically significant for delayed neurologic deficit. In this initial study we looked at preoperative and operative risk factors.

METHODS: We performed 854 thoracoabdominal aortic repairs between February 1991 and May 2001. For this study we excluded 26 patients who died before postoperative neurologic status could be evaluated and 38 who had immediate neurologic deficit on initial postoperative evaluation, leaving 790 consecutive patients. We evaluated a wide range of demographic, preoperative physiological and intraoperative data, using univariate and multivariable statistical analyses.

RESULTS: Twenty-one of 790 (2.7%) patients had delayed neurologic deficit. Significant univariate predictors included preoperative renal dysfunction (odds ratio 5.9; P < .006), acute dissection (odds ratio 3.9; P < .05), extent II thoracoabdominal aorta (odds ratio 3.0; P < .03), and use of adjuncts (cerebrospinal fluid drainage and distal aortic perfusion; odds ratio 7.7; P < .03). The use of the adjuncts dropped from the multivariable model but all other factors remained. No other significant risk factors were identified. Twelve of 21 (57%) patients recovered neurologic function with optimization of blood pressure and cerebrospinal fluid drainage.

CONCLUSION: Preoperative renal dysfunction, acute dissection, and extent II thoracoabdominal aorta are significant predictors of delayed neurologic deficit. Previous studies have demonstrated that the use of adjuncts protects against immediate neurologic deficit. The findings of this study are consistent with the hypothesis that adjuncts reduce ischemic insult enough to prevent immediate neurologic deficit but that a period of increased spinal cord vulnerability persists several days postoperatively.

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