Characterization of cerebrospinal fluid markers as indicators of spinal cord ischemia following an endovascular aortic aneurysm repair procedure

Objective: Spinal cord ischemia (SCI) remains one of the most devastating complications in both open and endovascular stent graft repair of thoracoabdominal aortic aneurysms. The endovascular aortic aneurysm repair (EVAR) can be either thoracic (TEVAR) when it targets the thoracic aortic aneurysm or fenestrated branched when repair involves the visceral and/or renal arteries. Even though EVAR interventions are less invasive than open repair, they are still associated with a significant risk of SCI. The current primary strategy to prevent SCI after TEVAR is to increase and/or maintain spinal cord perfusion pressure (blood flow) by increasing the mean arterial pressure while simultaneously draining CSF. Although the benefit of CSF drainage in EVAR procedures remains uncertain, it provides an opportunity to study the changes in cytokine and oxidative stress markers that may signal the pathophysiology of SCI following EVAR. The aim of this study was to evaluate the temporal relationship between stent deployment and CSF cytokine and oxidative stress marker levels as predictors of delayed SCI in patients undergoing an EVAR procedure.

Methods: There were 16 EVAR cases across 15 patients enrolled in this study, with 1 patient undergoing the procedure twice 1 year apart. The levels of oxidative stress (8-hydroxy-2'-deoxyguanosine [8-OHdG], glial fibrillary acidic [GFAP], and lactic acid) and proinflammatory (tumor necrosis factor-alpha [TNF-α], interleukin (IL)-6, and IL-1β) and antiinflammatory (IL-4) markers were quantified at different time points between 0 and 48 hours after EVAR by enzyme-linked immunosorbent assay. The changes in protein levels of both oxidative stress and inflammatory markers were expressed as fold change from the time of the lumbar drain insertion prior to surgery.

Results: Following the EVAR procedure, 8-OHdG resulted in the highest upregulation at later time points postoperatively (48 hours) and this increase was positively correlated with TNF-α level. The data also revealed that IL-6 peaked during the stent deployment intervention and this pattern of expression was positively correlated with the expression of lactic acid. No significant changes were noted in the expression levels of GFAP, lactic acid, and IL-1β.

Conclusions: There appears to be a temporal relationship between lumbar CSF drainage and CSF cytokines and oxidative stress markers that may help 1) identify patients at risk for developing delayed SCI and 2) modify patient management to prevent the damage from delayed SCI.