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Page 4 of 14 Monaco et al. Vessel Plus 2023;7:23 https://dx.doi.org/10.20517/2574-1209.2023.113

described the existence of a rich collateral pathway of vessels in both the perivertebral space and alongside
paraspinal muscles that anastomose outside the spinal canal, generating the spinal cord collateral network.
It consists of an axial network of small arteries in the spinal canal, perivertebral tissues, and paraspinal
muscles that anastomose with each other and with the nutrient arteries of the spinal cord. Inputs come from
segmental, subclavian, and hypogastric arteries and their branches (originating from the internal iliac artery,
namely the iliolumbar artery and lateral sacral arteries). Hence, the blood supply to the spinal cord can be
either increased from one source when another is reduced or decreased when a low-resistance pathway is
opened, leading to the steal phenomenon. This event is discernible and becomes apparent when utilizing an
aortic cross-clamp in the thoracic district while incising the aneurysmal thoracic aorta, as noted by
Christiansson and colleagues. Such action establishes a gradient between the spinal cord and the aorta,
causing retrograde bleeding from the intercostal arteries into the exposed aorta. As a result, this impacts the
spinal cord perfusion pressure (SCPP) and can potentially lead to anemia and hemodynamic instability .
[13]
Hence, there is the need to limit the back-flow from the intercostal arteries by the rapid insertion of
occlusive pegs, balloons, and tourniquets in the segmental vessels within the aorta. In particular,
Griepp et al. employed a method in which they clamp and divide the segmental vessels entering the aorta
within the segment to be excised prior to cross-clamping or opening the aorta, which resulted in a 2%
[14]
incidence of paraplegia . As virtually all clinical approaches to thoracic and thoracoabdominal aneurysm
resection unavoidably entail periods of cord ischemia, the importance of meticulous monitoring of
perfusion variables has become crucial to ensure sufficient blood flow through the spinal cord collateral
network.

Mechanisms of injury
From a pathophysiological perspective, an imbalance between oxygen demand and delivery (DO ) at the
2
spinal cord level following interruption of blood flow in the intercostal arteries during thoracic aortic
surgery causes SCI. Thoracic aorta cross-clamping leads to a reduction in perfusion pressure to the vascular
network supplying the central nervous system (CNS). Consequently, clamping time plays a pivotal role in
the development of ischemia since its lengthening triggers cellular and molecular alterations (e.g., shift from
aerobic to anaerobic metabolism), which in turn result in local and systemic alterations, ultimately leading
to ischemia. Noteworthy, the combination of both a direct (interruption of blood flow) and an indirect
effect which is in addition to the former (derived from the production of oxygen free radicals, lipid
peroxidation, intracellular calcium accumulation, leukocyte activation, inflammatory response) ultimately
results in neuronal apoptosis. More specifically, since visceral tissues in the district distal to the aortic clamp
shift from an aerobic to an anaerobic metabolism, lactates are produced and cellular membranes increase
their permeability, resulting in cellular swelling. Furthermore, the production of reactive oxygen species
(ROS) and nitric oxide (NO) coupled with lipid peroxidation suppress adenosine triphosphate (ATP)
synthesis, inactivate homeostatic metabolic enzymes, deplete antioxidant reserves, disrupt cellular and
mitochondrial membranes and further boost the phenomenon of apoptosis by means of intracellular
[15]
electrolytes derangement . All these factors acting simultaneously lead to the destruction of the blood-
spinal cord barrier, with spinal cord edema, increased leukocyte infiltration, amplification of inflammation,
and oxidative stress . Even reperfusion, causing inflammation, hyperemia, and edema, worsens overall
[16]
cellular damage and contributes to an irreversible clinical presentation of paraplegia. In daily clinical
practice, interrupting blood flow to the spinal cord does not always result in the development of SCI.
Furthermore, while reimplantation of intercostal arteries during TAAA repair is desirable, it is not always
feasible. Therefore, it might be plausible to replace an “anatomical paradigm” where sacrificing the
intercostal arteries inevitably leads to spinal cord ischemia with a “pathophysiological” paradigm, in which
spinal cord circulation is essentially ignored, and cardiac function, systemic arterial perfusion, DO , and
2
cellular metabolism become the therapeutic targets to prevent neurological damage [Table 1].