Prevention of spinal cord injury after repair of the thoracic or thoracoabdominal aorta

Michael C. Mauney, Lorne H. Blackbourne, Scott E. Langenburg, Scott A. Buchanan, Irving L. Kron, Curtis G. Tribble

Research output: Contribution to journalReview articlepeer-review

96 Scopus citations

Abstract

Spinal cord injury occurring as the result of surgical repair of thoracic and thoracoabdominal aortic disease remains a devastating complication. The incidence of postoperative neurologic deficits varies from 4% to 38%. Factors associated with a greater risk for injury include the presence of dissection or extensive thoracoabdominal disease, and a prolonged cross-clamp time. Spinal cord ischemia initiates a deleterious cascade of biochemical events that ultimately result in an increased intracellular calcium concentration. Calcium-activated proteases, lipases, and nucleases mediate the processes that cause cell injury. The accumulation of oxygen-derived free radicals and the occurrence of hyperemia during reperfusion are also contributing causes of spinal cord injury. Increasing the spinal cord blood flow with shunts, oxygenated bypass circuits, cerebrospinal fluid drainage, the intrathecal administration of vasodilators, and the reattachment of intercostal arteries has been tried in an effort to increase spinal cord perfusion. Pharmacologically based measures to prevent spinal cord injury have been pursued, and these have consisted of hypothermia, anesthetic agents, calcium channel blockers, free radical scavengers, and immune system modulation. However, no single technique has proved to be consistently effective in preventing ischemia-induced spinal cord injury.

Original languageEnglish (US)
Pages (from-to)245-252
Number of pages8
JournalThe Annals of Thoracic Surgery
Volume59
Issue number1
DOIs
StatePublished - Jan 1995
Externally publishedYes

ASJC Scopus subject areas

  • Surgery
  • Pulmonary and Respiratory Medicine
  • Cardiology and Cardiovascular Medicine

Fingerprint Dive into the research topics of 'Prevention of spinal cord injury after repair of the thoracic or thoracoabdominal aorta'. Together they form a unique fingerprint.

Cite this