Delayed spinal cord injury following electrical burns: a 7-year experience.

Although delayed spinal cord injury following high-voltage electrical burn is not a life-threatening sequelae, complete recovery is not the rule and the morbidity is high. In this study, we conducted a detailed analysis of clinical characteristics, radiographic findings and clinical outcomes in 13 patients with delayed spinal cord injury following electrical burns. The following features were notable. In 11 patients whose entry sites were the head and neck area, paraplegia was detected in cases whose exit sites were lower extremity only, while quadriplegia or cervical injury pattern EMG findings were observed in cases whose exit sites were upper extremity. Quadriplegia was also detected in cases whose exit sites were both upper and lower extremities. Quadriplegia was detected in one case whose entry site was hand and the exit site was the contralateral hand. Paraplegia was detected in one case in whom the entry site was the hand and exit site was the contralateral foot. In our patients, no complete loss of sensation was noted. Most of the patients were initially noted to have hypotonia between days 2 and 10 after electrical burn and were characterized by ascending paralysis, i.e., paraplegia followed by quadriplegia. We can postulate that these unique neurological manifestations after electrical injury may be due to the anatomical characteristics of the arterial blood supply of the spinal cord. The anterior gray matter, especially anterior horn cell is particularly susceptible to ischemic injury, because blood is supplied only by the sulcal branch, the longest branch originating from the anterior spinal artery. So, under the condition that all small sized vessels distributed in the spinal cord undergo degenerative change during a similar period of time, any occlusive event caused by thrombus or vascular wall injury in the sulcal branch will enhance the risk of ischemic injury in its distal area. Furthermore, the spinal cord at T4 to T8 levels is more vulnerable to ischemic injury due to poor collateral circulations. In conclusion, our postulates can explain the diverse patterns of delayed spinal cord injury, and enhance the rationale for early administration of prostaglandin E1 or steroid treatment to reduce ischemic spinal cord injury in cases of electrical burns.