After a spinal cord injury (SCI), evidence of insufficient oxygen levels and metabolic stress that can permanently damage tissue, persist for at least a week. It can also extend away from the injury site.
Evidence demonstrating hemodynamic and metabolic changes up to day 7 in a minipig model of traumatic SCI are reported in a new study published in Journal of Neurotrauma, a peer-reviewed journal from Mary Ann Liebert, Inc., publishers.
Brian Kwon and coauthors from University of British Columbia, Vancouver, suggest that the common clinical practice of providing patients with traumatic SCI with hemodynamic support out to 7 days post-injury may not be sufficient to prevent ischemia-related damage to the injured cord.
While the primary damage to the spinal cord occurs at the time of mechanical impact (e.g., from a motor vehicle accident, fall from height), early treatment approaches for the acutely injured patient aim to mitigate the secondary pathophysiologic processes that are triggered within the injured cord.
These include vascular disruption, intraparenchymal hemorrhage, vasospasm, impaired autoregulation, and vasogenic edema as a consequence of blood-spinal cord barrier breakdown. These combined responses can lead to impaired spinal cord perfusion with resultant ischemia, hypoxia, and energy dysfunction, of which all can negatively impact spared neural tissue at and around the injury site.
Therefore, current clinical practice guidelines encourage aggressive hemodynamic resuscitation and elevation of mean arterial blood pressure (MAP) to 85-90 mm Hg for the first 7 days post-injury.
"This is an important paper reporting on preclinical findings using a large animal model that could impact how physicians manage SCI patients," says W. Dalton Dietrich, PhD, Deputy Editor of Journal of Neurotrauma and Professor, University of Miami Miller School of Medicine, Miami, Florida.
"The results indicate that providing hemodynamic support to SCI patients for a restricted period may not be optimal to protect against posttraumatic injury mechanisms."