Detrimental effects of cerebrospinal fluid pressure elevation on spinal cord perfusion: first-time direct detection in a large animal model

Abstract

OBJECTIVES: Cerebrospinal fluid (CSF) drainage is routinely utilized to mitigate perioperative and postoperative spinal cord ischaemia in open and endovascular thoraco-abdominal aortic aneurysm repair to prevent permanent paraplegia. Clinical decision-making in the vulnerable perioperative period, however, is still based on limited clinical and experimental data. Our aim was to investigate the isolated effect of CSF pressure elevation on spinal cord perfusion in an established large animal model. METHODS: Ten juvenile pigs with normal (native) arterial inflow (patent segmental arteries and collaterals) underwent iatrogenic CSF pressure elevation (x2, x3, x4 from their individual baseline pressure). Each pressure level was maintained for 30min to mimic clinical response time. After the quadrupling of CSF pressure, the dural sac was slowly depressurized against gravity allowing CSF pressure to passively return to baseline values. Measurements were taken 30 and 60min after normalization, and microspheres for regional blood flow analysis were injected at each time point. RESULTS: Spinal cord perfusion decreased significantly at all mid-thoracic to lumbar cord segments at the doubling of CSF pressure and declined to values <53% compared to baseline when pressure was quadrupled. Normalizing CSF pressure led to an intense hyperperfusion of up to 186% at the cervical level and 151% within the lumbar region. CONCLUSIONS: CSF pressure elevation results in a relevant impairment of spinal cord blood supply. Close perioperative and postoperative monitoring of CSF pressure is crucial for maintaining sufficient spinal cord perfusion. Radical and rapid withdrawal of CSF is followed by significant hyperperfusion in all spinal cord segments and may lead to 'drainage-related' iatrogenic reperfusion injury-aggravating the risk of delayed spinal cord injury-and should therefore be avoided.