Con: Retrograde cerebral perfusion is not an optimal method of neuroprotection in thoracic aortic surgery.

As the utility of retrograde cerebral perfusion (RCP) as a method of neuroprotection for thoracic aortic surgery is considered, it is useful to review the rationale underlying its use. Proponents of the technique use RCP because it is believed to increase the tolerance of the brain to longer periods of interruption of anterograde flow by some combination of metabolic support, maintenance of cerebral hypothermia, and clearing of embolic material from the cerebrovascular system. Not all of these assertions, however, are well supported in the literature. In a recent review of this topic, most rigorous studies do not support the ability of RCP to provide cerebral metabolic support or to flush emboli from the cerebral circulation.1 Ideally, clinical outcome studies evaluating the efficacy of RCP as a neuroprotective technique should use random assignment of patients to either hypothermic circulatory arrest (HCA) or RCP groups to reduce the influence of confounding factors such as: severity of aortic disease; surgical complexity; total time of interrupted anterograde cerebral flow; and improvements in surgical, anesthetic, and perfusion techniques that occur over time. For practical reasons, however, no such studies have been performed, and the majority of clinical reports are case series with historical controls. Studies assessing postoperative neurologic morbidity and the neuroprotective efficacy of RCP have examined the incidence of 3 different cerebral complications: stroke, temporary neurologic dysfunction, and decline in cognitive test scores. Studies comparing stroke rates have found either no difference between HCA and RCP patients2,3 or lower rates with RCP.4-6 Studies examining the association between RCP duration and stroke rates have found no statistically significant relationships.7-9 Strokes associated with thoracic aortic surgery are most often embolic in nature and are thought to occur during aortic and arch vessel manipulations, such as cross-clamping, cannulation, and anastomoses of graft material to atherosclerotic vessels. It is not likely that RCP would ameliorate this type of injury unless it is capable of flushing embolic material from the cerebrovascular tree before irreversible injury. The 1 animal study that showed removal of cerebral microemboli by RCP resulted in histopathologic injury and severe behavioral dysfunction postoperatively.10 There is no evidence-based literature to support the ability of RCP to flush macroemboli from the cerebral circulation. Far more common than stroke, nonfocal temporary neurologic dysfunction, consisting of confusion, agitation, delirium, and prolonged obtundation, is frequently associated with thoracic aortic surgery, especially in the elderly.11 Temporary neurologic dysfunction is believed to reflect inadequate cerebral protection from global ischemia because the incidence increases with duration of circulatory arrest. At the authors’ institution, an assessment of temporary neurologic dysfunction is routinely performed in patients surviving surgery for at least 24 hours. In a recent study of 91 patients with 40 to 80 minutes of interrupted anterograde cerebral blood flow, there was less temporary neurologic dysfunction in those having selective cerebral perfusion than in those having either HCA alone or HCA with RCP (odds ratio 0.3, p 0.048).9 The incidence of temporary neurologic dysfunction was 69.2% in RCP patients and 52.9% in patients having HCA alone, but this finding was not statistically significant. The most sensitive measure of postoperative cerebral injury is neuropsychological testing, which involves the evaluation of cognitive functions such as attention, processing speed, language, memory, and executive functions. The authors recently compared neuropsychological outcome in 12 RCP patients and 44 HCA patients. Relative to HCA, RCP was associated with memory dysfunction and an overall increase in neuropsychological dysfunction in multiple domains, controlling separately for the effects of age and cerebral ischemia time.12 Looking to the future, centers that perform RCP may reduce the confounding effects of the learning curve by incorporating year of operation in the multivariate model for determining the predictors of adverse outcomes after RCP. This may enable the separation of the effects of the learning curve from that of RCP itself as surgeons became more proficient over time. Another problem with the existing literature is that patients differ in their relative risk for cerebral injury. Patients who require complex repairs of the aortic arch are at higher risk of persistent postoperative cognitive dysfunction. In the initial work in this area, there was no difference in cognitive outcome between ascending aortic repairs treated with HCA alone and coronary artery and valve surgery patients with no HCA, whereas the patients who underwent longer periods of HCA (aortic arch repairs) had persistently worse memory and fine motor function postoperatively.13 It is not clear whether the duration of HCA or some other factor led to worse outcomes in the aortic arch repair patients. Other risk factors, such as friable atheromatous aortic plaque (“dirty aorta”) and age, must also be considered in these comparative analyses. The common practice of mixing data from patients with relatively brief interruptions of anterograde perfusion (ascending aortic repairs) with the more complex aortic arch repairs dilutes the impact of the higher risk patients and biases the results of comparative trials to findings of “no difference” because of the greater prevalence of simpler aortic repairs in clinical practice. Given the small numbers of cases involved and the confounding factors noted earlier, future studies of RCP’s putative neuroprotection must control for the complexity of the surgical repair (duration of the period of aortic From the Department of Anesthesiology, Mount Sinai School of Medicine, New York, NY. Reprints not available. Address correspondence to David L. Reich, MD, Department of Anesthesiology, Box 1010, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029-6574. E-mail: david.reich@msnyuhealth.org © 2003 Elsevier Inc. All rights reserved. 1053-0770/03/1706-0019$30.00/0 doi:10.1053/j.jvca.2003.09.021