4.6 Article Proceedings Paper

Effect of cerebrospinal fluid pressure elevation on spinal cord perfusion during aortic cross-clamping with distal aortic perfusion

Journal

EUROPEAN JOURNAL OF CARDIO-THORACIC SURGERY
Volume 60, Issue 3, Pages 569-576

Publisher

OXFORD UNIV PRESS INC
DOI: 10.1093/ejcts/ezab167

Keywords

Spinal cord injury; Distal perfusion; Paraplegia; Paraparesis; Collateral network

Funding

  1. European Union's Horizon 2020 research and innovation programme [733203]
  2. German Research Foundation [127/2-1]
  3. H2020 Societal Challenges Programme [733203] Funding Source: H2020 Societal Challenges Programme

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The study evaluates the effects of distal aortic perfusion (DaP) on regional spinal cord blood flow during descending aortic cross-clamping and iatrogenic elevation of cerebrospinal fluid pressure. DaP leads to hyperperfusion of the distal spinal cord but does not provide adequate flow to upper and middle spinal cord segments, and is unable to counteract an experimental cerebrospinal fluid pressure elevation, resulting in decreased blood flow to certain spinal cord segments.
OBJECTIVES: Distal aortic perfusion (DaP) is a widely accepted protective adjunct facilitating early reinstitution of visceral perfusion during extended thoracic and thoraco-abdominal aortic repair. DaP has also been suggested to secure distal inflow to the paraspinal collateral network via the hypogastric arteries and thereby reduce the risk of spinal cord ischaemia. However, an increase in cerebrospinal fluid (CSF) pressure is frequently observed during thoracoabdominal aortic aneurysm repair. The aim of this study was to evaluate the effects of DaP on regional spinal cord blood flow (SCBF) during descending aortic cross-clamping and iatrogenic elevation of cerebrospinal fluid pressure. METHODS: Eight juvenile pigs underwent central cannulation for cardiopulmonary bypass according to our established experimental protocol followed by aortic cross-clamping of the descending thoracic and abdominal aorta-mimicking sequential aortic clamping-with the initiation of DaP. Thereafter, CSF pressure elevation was induced by the infusion of blood plasma until baseline CSF pressure was tripled. At each time-point, microspheres of different colours were injected allowing for regional SCBF analysis. RESULTS: DaP led to a pronounced hyperperfusion of the distal spinal cord [SCBF up to 480%, standard deviation (SD): 313%, compared to baseline]. However, DaP provided no or only limited additional flow to the upper and middle segments of the spinal cord (C1-Th7: 5% of baseline, SD: 5%; Th8-L2: 24%, SD: 39%), which was compensated by proximal flow only at C1-Th7 level. Furthermore, DaP could not counteract an experimental CSF pressure elevation, which led to a further decrease in regional SCBF most pronounced in the mid-thoracic spinal cord segment. CONCLUSIONS: Protective DaP during thoraco-abdominal aortic repair may be associated with inadequate spinal protection particularly at the mid-thoracic spinal cord level ('watershed area') and result in the adverse effect of a potentially dangerous hyperperfusion of the distal spinal cord segments.

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