Is Retrograde Cerebral Perfusion an Effective Means of Neural Support During Deep Hypothermic Circulatory Arrest

As surgical mortality and morbidity from cardiac and aortic operations have steadily improved over the past decade, interest has increasingly been directed toward the cerebral sequelae of these operations. In adults, it has become apparent that focal embolic events are the most frequent cause of serious permanent neurologic morbidity and subsequent mortality, but that at least transient diffuse cerebral dysfunction occurs in a large proportion of patients [1, 2]. In children with congenital heart disease, in whom operation is now carried out most frequently in the neonatal period and often requires prolonged hypothermic circulatory arrest (HCA), disturbing evidence is accumulating that later intellectual function may be compromised [3]. The recognition that cerebral function after cardiac or aortic operations is frequently impaired at least transiently has led to reevaluation of techniques for cerebral protection, especially when the operation requires interruption of antegrade flow. A consensus has emerged that prolonged durations of HCA are a frequent risk factor for later cerebral dysfunction [3, 4], fueling a search for alternatives to HCA and for adjuncts that would increase its safety. Among these, retrograde cerebral perfusion (RCP) has become very popular and has been adopted for clinical use, especially in aortic surgery, despite the fact that very little convincing evidence exists to document either its efficacy or safety. Enthusiasm for RCP stems from its appeal as a possible way of reducing embolic injury in addition to its potential usefulness in improving cerebral protection during HCA. Although a number of clinical studies extol the virtues of RCP, many suffer from serious shortcomings: the typical report includes fewer than 50 patients, the majority of whom had RCP for short intervals, which should have resulted in a good outcome with HCA alone [5–10]. Although ostensibly evaluating cerebral protection, none of these studies involve formal psychometric evaluation, and most make no distinction between permanent and temporary neurologic dysfunction or between focal and diffuse cerebral injury: they simply cite the incidence of permanent neurologic damage and perhaps compare this with unmatched historical controls. But because most permanent neurologic injury after aortic operations is focal in nature, and therefore is likely to be embolic in origin [1, 2], its occurrence is probably only marginally related to the adequacy of cerebral protection. This is in contrast with the relatively more frequent syndrome of prolonged postoperative obtundation and confusion, which rarely results in obvious permanent sequelae but is clearly more prevalent with longer durations of HCA [1, 2] and is therefore a much more sensitive and appropriate indicator of the extent of cerebral protection. The theoretical appeal of RCP and the failure of clinical studies to answer vital questions about its possible benefits and risks prompted us to undertake a series of laboratory investigations [11–13]. These studies have convinced us that although RCP has promise for improving cerebral outcome after HCA, there is also potential for harm associated with its use.