Elsevier

Journal of Vascular Surgery

Volume 20, Issue 3, September 1994, Pages 434-443
Journal of Vascular Surgery

Neurologic deficit in patients at high risk with thoracoabdominal aortic aneurysms: The role of cerebral spinal fluid drainage and distal aortic perfusion*,**

Presented at the Eighteenth Annual Meeting of the Southern Association for Vascular Surgery, Scottsdale, Ariz., Jan. 26-29, 1994.
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Abstract

Purpose: This prospective study evaluated the possible prevention of postoperative neurologic deficit in patients at high risk with thoracoabdominal aortic aneurysms (TAAA), types I and II, by use of perioperative cerebrospinal fluid drainage and distal aortic perfusion. Methods: Between September 18, 1992, and August 8, 1993, 45 consecutive patients underwent TAAA repair (14 type I, 31 type II). Thirty-six were men and nine were women. The median age was 63 years (range 28 to 88). Twenty-four of 45 patients (53%) had dissection and 17 of 45 (38%) had prior proximal aortic replacement. All patients underwent perioperative cerebrospinal fluid drainage and distal aortic perfusion. Median aortic clamping time was 42 minutes. Thirty-five of 45 patients (78%) underwent intercostal artery reattachment. Results: The 30-day survival rate was 96% (43 of 45 patients). Early neurologic deficit occurred in two of 45 patients (4%), and late neurologic deficit also occurred in two of 45 patients (4%). We compared the neurologic deficit of our current group of 45 patients with the data of a previously unpublished study of 112 patients also from this center. Total neurologic deficit for the current group was four of 45 (9%) versus the previous group of 35 of 112 (31%) with a p value of 0.0034 (Pearson chi-square test). Neurologic deficit for patients with type I TAAA was 0 of 14 (0%) versus 15 of 73 (21%) (p = 0.062); for patients with type II TAAA 4 of 31 (13%) versus 20 of 39 (51%) (p = 0.0008). In patients with aortic dissection, neurologic deficit was 3 of 24 (12%) versus 9 of 32 (28%) (p = 0.0304); no dissection was 1 of 21 (5%) versus 26 of 80 (32%) (p = 0.011). For aortic clamp times less than 45 minutes, neurologic deficit was 1 of 24 (4%) versus 14 of 68 (21%) (p = 0.061); for aortic clamp times equal to or greater than 45 minutes, neurologic deficit was 3 of 21 (14%) versus 21 of 44 (48%) (p = 0.0090). Conclusion: Neurologic deficit in patients treated for types I and II TAAA was reduced significantly by perioperative cerebral spinal fluid drainage and distal aortic perfusion. (J VASC SURG 1994;20:434-43.)

Section snippets

MATERIAL AND METHODS

We based our prospective study on 45 consecutive patients treated for type I or type II TAAA repair between September 18, 1992, and August 8, 1993. There were 36 male and nine female patients. The median age was 63 years (range 28 to 88 years). Fourteen patients (31%) had type I TAAA, and 31 (69%) had type II TAAA. With regard to cause, aneurysms were due to dissection in 24 patients (53%) (3 acute type III, 13 chronic type I, and 10 chronic type III). In 17 patients (38%), aneurysms were due

RESULTS

All patients survived operative repair of TAAA. The 30-day mortality rate was 2 patients out of a total of 45 (4%). Intraoperative cardiac arrest developed in one patient. He was successfully resuscitated, but awoke with paraplegia. Kidney failure also developed in him. The patient and his family opted for withholding the life support systems and subsequently he died. The second patient had successful type II TAAA repair and was discharged from the hospital. Twenty-eight days later he was

DISCUSSION

Perfusion pressure of the spinal cord equals spinal arterial pressure minus CSF pressure. 19 During aortic clamping, in addition to the hemodynamic effect on the heart, distal aortic pressure decreases dramatically, leading to a decrease in spinal arterial pressure. 20 Tissue pressure as measured by CSF pressure increases, markedly compromising the perfusion pressure of the spinal cord.

We chose the combined methods of CSFD and DAP for our current prospective study based on the hypothesis that,

Acknowledgements

We gratefully acknowledge Amy Wirtz Newland for editorial assistance.

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*

Reprint requests: Hazim J. Safi, MD, 6550 Fannin, Suite 1603, Houston, TX 77030.

**

0741-5214/94/$3.00 + 24/6/57551

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