Hemodynamic Management of Acute Spinal Cord Injury

Acute traumatic spinal cord injury primarily afflicts young people and significantly reduces independence, bestows life-long disability, and consumes huge societal resources. The estimated incidence of acute traumatic spinal cord injury in North America varies from 27–81 cases per million inhabitants per year [1]. The prevalences of spinal cord injury were estimated to be 280 and 681 individuals per million inhabitants in Finland and Australia, respectively. Despite recent efforts at prevention, including laws mandating seat belt use, the incidence of spinal cord injury has not changed significantly andmay actually be increasing in certain parts of the population [2, 3]. In addition, the estimated (2006) treatment cost of spinal cord injury is $9.7 billion per year [1]. A number of pharmacological agents (methylprednisolone sodium succinate, and the related compound, tirilazad mesylate; GM-1 ganglio-side; thyrotropin-releasing hormone; gacyclidine; naloxone; and nimodipine) have been investigated in large, prospective, randomized, controlled clinical trials, but all have failed to demonstrate convincing neurological benefit. Spinal cord injury is frequently associated with systemic hypotension attributable to hypovolemia, direct spinal cord trauma, or both [4].