Paralysis after aortic surgery: in search of lost cord function.

During the early 1980s, the rate of paralysis after aortic surgery was as high as 41% in patients for the most complex thoracoabdominal aortic operations. After comparing human and chacma baboon (papio ursinus) spinal cord vascular anatomy, an animal model was established to study the pathophysiology of aortic cross-clamping and the aetiology of the paralysis. Techniques, including motor evoked responses for monitoring spinal cord function, were developed that were tried in humans and later culminated in prospective and randomized studies. These established that the following were protective: combining cerebrospinal fluid with intrathecal papaverine; cooling systemically to moderate or profound hypothermia; minimizing intercostal ischaemia time; using a sequential segmental repair approach; re-attaching all patent and segmental intercostal arteries below T8 for descending thoracic aortic repair and from T6 to L2 for thoracoabdominal repairs; continuing cerebrospinal fluid drainage for at least two days and maintaining patients hypertensive after surgery. The net result has been that, in two of our recent series, the risk of permanent paralysis has been reduced to between 3.1% and 3.8%.