Cerebral protection in type A aortic dissection

Abstract

: Acute type A aortic dissection (ATAD) carries extremely high morbidity and mortality with a significantly increased risk of cerebrovascular injury following repair compared to elective arch operations. Advancement in operative and neuroprotective strategies have led to a temporal improvement in outcomes, but the incidence of cerebrovascular injury remains high and warrants continued innovation. In the setting of ATAD, stroke can occur due to malperfusion resulting from true lumen compression and compromised cerebral inflow, malperfusion from cardiogenic shock, or embolization. Therefore, stroke mitigation strategies must address vascular obstructions, hemodynamic compromise, and reduce risk of embolization. This article reviews contemporary strategies for cerebral protection in ATAD including preoperative patient evaluation, perfusion and temperature management, extent of aortic repair, utility of cerebral oximetry and neuromonitoring, and pharmacological adjuncts. In summary, patients should be evaluated preoperatively with contrast imaging to fully characterize their dissection to facilitate well-informed operative planning. Cannulation for cardiopulmonary bypass (CPB) can be safely achieved through multiple routes, but should consider patient pathology and the intended approach to cerebral perfusion. Central cannulation is feasible in most patients and allows for the most expeditious initiation of CPB. Although both deep hypothermic circulatory arrest (HCA) with retrograde cerebral perfusion (RCP) and moderate HCA with antegrade cerebral perfusion (ACP) have been shown to provide adequate cerebral protection, targeting moderate hypothermic temperatures reduces CPB times. The combination of a brief period of RCP followed by ACP during moderate HCA allows for the potential flushing of emboli from the cerebral arterial system with the superior metabolic protection of antegrade perfusion. The proximal and distal extent of arch repair should be individually tailored to patient pathology and surgeon experience, making sure to completely resect disease to prevent acute neurological complications. Cerebral oximetry and neuromonitoring are useful adjuncts, providing real-time information about the adequacy of neuroprotection. Finally, co-management by anesthesiologists and perfusionists with administration of neuroprotective agents, appropriate pH management, and maintenance of normal metabolic hemostasis and hemodynamic stability will further minimize cerebrovascular complications. Optimal cerebral protection requires a comprehensive, interdisciplinary approach and implementation of multimodal strategies.