Abstract
ESPITE recent advances in anesthetic, surgical, and monitoring techniques, ischemic complications due to aortic cross-clamping continue to occur. The most devastating and unpredictable complication following surgery of the descending and thoracoabdominal aorta is paraplegia. This complication ranges from 0.5% to 38%.*-6 Cross-clamping of the proximal descending aorta interrupts the blood supply to the area supplied by the aortic segment distal to the clamp. Prolonged clamping results in the catastrophic complication of paraplegia. The duration of this ischemia is the single most important factor affecting the incidence of paraplegia.’ Cunningham et al7 reported that ischemic periods associated with less than 30 minutes of somatosensory evoked potential (SEP) loss did not result in paraplegia, whereas longer periods of ischemia resulted in a 71% incidence of paraplegia. Hollier8 stated that a shunt is unnecessary for spinal cord protection if aortic cross-clamp time is kept below 30 minutes. Kobrine et al9 demonstrated that the long tract neural conduction in the spinal cord appeared quite refractory to the effects of ischemia and disappeared after 8 to 18 minutes of absolute ischemia. Tarlovl” reported loss of spinal evoked potentials within 18 minutes of spinal cord ischemia following occlusion of the descending thoracic aorta. Katz et ali1 studied 35 patients with traumatic aortic transection. They reported that spinal cord injury was more likely to occur with long aortic cross-clamp times and when no shunt was used to perfuse the distal aortic segment during aortic crossclamping. They suggested that if the aortic cross-clamp time is to exceed 30 minutes, a shunt should be used during aortic cross-clamping. In an analysis of 360 patients operated on for resection of a descending thoracic aneurysm, Livesay et all2 documented that there is a low risk of paraplegia (3%) when the aortic cross-clamp time is less than 30 minutes. In the same study, they reported that after more than 30 minutes of aortic cross-clamping, there was a significant rise in the risk of paraplegia (10%). Slager13 reported that spinal cord electrical function ceases after 30 to 90 seconds of total anoxia. Reporting on the anterior spinal artery syndrome, Zuber and Casper14 pointed out that transient damage of the spinal cord occurs after 15 minutes of vascular occlusion and permanent damage after 20 minutes or more of total anoxia. Conversely, Crawford and Rubio15 demonstrated no clear relationship between cross-clamp time and the incidence of paraplegia. The relationship between the aortic cross-clamp time and the probability of paraplegia is the function of a sigmoid curve (Fig 1) as shown in the studies of Katz et all6 and Jex et al.” In patients with high-risk aortic lesions, it is clear that if the thoracic aortic cross-clamping is less than 30 minutes, the risk of paraplegia is small.‘* Nevertheless, the authors have seen paraplegia occur with a 13-minute aortic cross-clamp time. In the authors’ view, between 30 and 60 minutes vulnerability to paraplegia exists, and the risk of paraplegia increases steeply with time.ls At 60 minutes, the risk of paraplegia approaches 90%. The curve is shifted to the right with lower risk aortic surgery and by protective measures, thus prolonging the period of safetyls (Fig 1). Other factors play a role in ischemic spinal cord injury. These include variations in the blood supply of the spinal cord and the state of the collateral circulation; the nature of the disease; the length of the aortic segment involved in the aneurysmal process; the level of blood pressure and cerebrospinal fluid pressure; and the use of sodium nitroprusside during surgery.‘* The Blood Supply of the Spinal Cord
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