Short Communication
Spinal Cord Injury during Thoracic Endovascular Aneurysm Repair
Taijiro Sueda* and Shinya Takahashi
Department of Cardiovascular Surgery, Hiroshima University, Japan
*Corresponding author: Taijiro Sueda, Department of Cardiovascular Surgery, Hiroshima University Graduate School of Medicine, 1-2-3, Kasumi, Minami-ku, Hiroshima, 734-8551, Japan
Published: 20 Sep, 2017
Cite this article as: Sueda T, Takahashi S. Spinal Cord
Injury during Thoracic Endovascular
Aneurysm Repair. Clin Surg. 2017; 2:
1627.
Short Communication
Spinal cord injury (SCI) is a devastating complication of thoracic aortic aneurysm repair.
Thoracic endovascular aneurysm repair (TEVAR) is a less invasive treatment for thoracic aortic
aneurysm repair. This short communication describes the recent knowledge of SCI during TEVAR.
Two theories have been proposed to explain spinal cord circulation: one based on anatomy
(intercostal or lumbar arteries) and one based on a dynamic demand-dependent (collateral) blood
supply. Understanding the anatomy of spinal cord blood supply is essential for developing strategies
to prevent SCI. In 1881, Albert W. Adamkiewicz suggested that the most important input to the
ASA is a single dominant branch of a segmental artery in the thoracic or upper lumbar region,
now referred to as the artery of Adamkiewicz [1]. Adamkiewicz’s concept became the predominant
theory and rationale for their implantation of intercostal and lumbar arteries, each arising from
the regional segmental arteries and, supplying the cervical, thoracic and lumbosacral regions of
the spinal cord. However, Adamkiewicz’s idea has proven to be controversial: opponents argue
that reimplantation of the segmental arteries during thoracic aortic aneurysm repair is the best
strategy for preserving spinal cord blood flow to the spinal cord. Despite attempts to avoid SCI
with this approach, there continues to be a definite, irreducible incidence of SCI after extensive
thoracoabdominal aortic aneurysm repair Reattachment of the intercostal and lumbar segmental
arteries is not possible during TEVAR, but the incidence of SCI after TEVAR is lower than that
after open surgery. It has been hypothesized that an axial network of small arteries feeds the spinal
canal, perivertebral tissues and paraspinal muscles and receives input from the subclavian, internal
thoracic, lumbar and hypogastric arteries [2]. These small arteries are interconnected and are also
connected with the anterior and posterior spinal arteries and provide blood flow to the spinal
cord. This arterial network allows for increased blood flow from one source when another source
is impaired. Spinal cord blood flow is reduced if an alternative, lower resistance pathway becomes
patent elsewhere in the circulation.
Independent risk factors for the development of delayed onset SCI include a perioperative mean
arterial pressure of less than 70 mmHg, complications of CFS drainage, previous abdominal aortic
aneurysm repair (if the hypogastric arteries have been compromised), significant preoperative renal
failure, left subclavian artery coverage without revascularization, and the use of multiple stent-grafts
(coverage of a long segment). However, the simultaneous closure of two independent arterial spinal
cord vessels, particularly when combined with intraoperative hypotension, has been shown to be
the most important risk factor for symptomatic SCI, irrespective of the covered length or previous
aortic repair, reinforcing the importance of the collateral arterial network.
The risk of SCI resulting from TEVAR may be decreased by with cerebrospinal fluid (CSF)
drainage [3]. In clinical studies, CSF pressure reduction has been shown to increase spinal cord
perfusion pressure. However, there is still no consensus on the role of CSFD in TEVAR. Coverage
of the left subclavian artery compromises the proximal collateral circulation to the vertebral and
internal thoracic arteries. Coverage of long segments of the thoracic aorta using more than two
stent grafts also limits spinal cord perfusion by compromising important intercostal and lumbar
segmental arteries supplying the anterior spinal cord artery. Prior AAA surgery diminishes spinal
cord perfusion by compromising pelvic and hypogastric collaterals. Other independent risk factors
include age, number of patent lumbar arteries, emergency surgery, prolonged duration of the
procedure and iliac artery injury. Postoperative hypotension and increased cerebrospinal fluid
pressure are also associated with the increased risk of neurologic deficits after TEVAR. These results
are predictable based on the physiological principle that spinal cord perfusion pressure is equal to
the difference between the mean atrial pressure and the cerebrospinal fluid pressure. Blood pressure augmentation and waking the patient early from anesthesia can help us detect signs of SCI. When SCI is detected, CSF drainage and arterial
blood pressure augmentation can prevent delayed SCI. Coverage of
the thoracic aorta by TEVAR and the exclusion of relevant segmental
arteries are associated with relatively low rates of SCI, suggesting that
an exclusively anatomical explanation of SCI is inadequate. Collateral
arterial networks, anesthesia stability, and the duration of ischemia
are all important contributing factors. Despite advances in our
understanding of spinal cord perfusion, postoperative SCI remains
a serious and challenging complication of thoracic aortic aneurysm
repair.
References
- Adamkiewicz A. Die Blutegefaesse des mecanichen Rueckenmarks, SB Heidelberg Akad Wiss. 1882; Theil I+II:101-30.
- Griep RB, Ergin MA, Galla JD, Lansman S, Khan N, Quintana C, et al. Looking for the artery of Adamkiewicz: a quest to minimize paraplegia after operations for aneurysms of the descending thoracic and thoracoabdominal aorta. J Thorac Cardiovasc Surg. 1996;112:1202-12;13-5.
- Bobadilla JL, Wynn M, Tefera G, Acher CW. Low incidence of paraplegia after thoracic endovascular aneurysm repair with proactive spinal cord protective protocols. J Vas Surg. 2013;57(6):1537-42.