Con: cerebrospinal fluid drainage does not protect the spinal cord during thoracoabdominal aortic reconstruction surgery.

PARAPLEGIA RESULTING from ischemic spinal cord injury is the most feared complication associated with thoracoabdominal aortic aneurysm (TAAA) repair. This unpredictable complication is associated with decreased survival and devastating physical disability.1,2 The incidence of permanent or transient paraplegia or paraparesis after aortic aneurysm repair was reported in the early 1990s by Svensson et al1 to range from 4% for type IV TAAAs to 31% for type II TAAAs. Factors associated with postoperative paraplegia or paraparesis include aneurysm extent, acute dissection, rupture, previous aortic surgery, aortic cross-clamp time, diabetes, and preoperative renal dysfunction.1 Spinal cord injury after TAAA repair is largely determined by (1) the duration and degree of spinal cord ischemia, (2) failure to reestablish an adequate blood supply, and (3) a biochemically mediated reperfusion injury as a result of the ischemia.3 Strategies aimed at reducing neurologic complications have focused on these 3 areas. Many methods of spinal cord protection that have proved beneficial in animals have been disappointing in humans. To date, no method or combination of methods of spinal cord protection has been totally effective in preventing postoperative neurologic deficits. Methods currently advocated include distal arterial perfusion (atriofemoral or femorofemoral bypass); reattachment of intercostal arteries; generalized hypothermia; local hypothermia; medications such as barbiturates, naloxone, steroids, and papaverine; and cerebrospinal fluid (CSF) drainage.2 Cross-clamping of the aorta decreases perfusion of the spinal cord by simultaneously increasing CSF pressure and decreasing distal aortic perfusion pressure. Decreasing CSF pressure with CSF drainage theoretically should increase spinal cord perfusion. In 1962, Blaisdell and Cooley4 showed an improved neurologic outcome using CSF drainage in a model of spinal cord ischemia in dogs. Although much has been published concerning intraoperative and postoperative CSF drainage in humans, the hypothesis that CSF drainage reduces the incidence of neurologic deficits is controversial. The use of CSF drainage has never been investigated in a multicenter, randomized controlled trial. In 2000, Ling and Arellano5 published a systematic overview of the evidence supporting the use of CSF drainage in TAAA surgery for prevention of paraplegia. The authors concluded, “No intervention has yet been proven to reduce the incidence of neurologic deficits after TAAA repair.. . . The role of CSF drainage for prevention of delayed-onset deficits caused by late spinal cord edema postoperatively also remains undetermined.”5 Most of the nonrandomized studies in the literature advocate CSF drainage as part of a strategy to minimize spinal cord injury. However, many potential sources of systematic and random error in these studies make it difficult, to interpret the role of CSF drainage in spinal cord protection.5 Of the 3 published randomized controlled trials of CSF drainage to reduce neurologic injury, the study by Crawford et al in 19916 failed to show a benefit, and the study by Svensson et al in 19987 is difficult to interpret because of confounding factors. The use of CSF drainage for reducing neurologic deficits during TAAA repair currently is supported only by the randomized controlled trial of Coselli et al.2 In a nonrandomized historical cohort study by Murray et al in 1993,8 no improvement in neurologic outcome was found using CSF drainage to keep CSF pressure 15 mmHg. This result may reflect either a lack of power to determine an actual effect of CSF drainage or inadequate lowering of CSF pressure in the study. It is possible that a positive finding was masked because more type II TAAAs, those at highest risk, were included in the intervention group.5 Other nonrandomized studies by Hollier et al in 1992,9 Archer et al in 1994,10 and Safi et al in 199611 purportedly showed a benefit to CSF drainage during TAAA repair. However, these observational cohort and historical control studies had major methodologic limitations. In reference to these studies, Ling and Arellano5 stated, “variability in treatment and control populations, intervention, and distribution of confounders (ie, surgical technique) possibly affected the outcome. Furthermore, bias in the trial designs may exaggerate the treatment effect. Detail on the neurologic evaluation was not provided in any study” and all of these studies were retrospective. In particular, it is difficult to assess the role of CSF drainage in the study by Archer et al10 because the intervention group received combined CSF drainage and intravenous naloxone, and the control group consisted of a heterogenous group of patients, including patients who had received CSF drainage alone, naloxone alone, or neither CSF drainage nor naloxone. The first randomized controlled trial of CSF drainage, reported by Crawford et al6 in 1991, failed to show a reduction in neurologic deficits after TAAA repair. Although this study was well designed, the Institutional Review Board limited CSF drainage to 50 mL, which may account for the failure to show its benefit. In 1998, Svensson et al7 reported on another randomized controlled trial involving the use of CSF drainage. Patients in the treatment group received CSF drainage and intrathecal papaverine, however. Other adjuncts, such as left heart bypass and active cooling, were used inconsistently in the treatment and control groups. It is not possible to interpret the impact of CSF drainage alone in this study. This study was terminated after only one third of the estimated sample size had been enrolled because of a statistically significant difference in the rate of neurologic deficit between groups (p 0.039). Ling and Arellano5 concluded that it is probable their conclusion is based on type I error because a “p value of 0.039 would not be considered statistically significant for an interim analysis of a clinical trial, and it is unfortunate that the trial was terminated early based on this result.” Coselli et al2 reported on a randomized controlled trial of CSF drainage to reduce neurologic injury after type I or type II TAAA repair. In this study, From the Department of Cardiothoracic Anesthesia, The Cleveland Clinic Foundation, Cleveland, OH. Address reprint requests to Lee Wallace, MD, Department of Cardiothoracic Anesthesia/G-30, The Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195. E-mail: wallacl@ccf.org Copyright 2002, Elsevier Science (USA). All rights reserved. 1053-0770/02/1605-0024$35.00/0 doi:10.1053/jcan.2002.126934