Abstract

The pathogenesis of spinal cord ischaemia following open surgical repair of thoracoabdominal aortic aneurysms (TAAAs) has been established over many years and includes spinal cord ischaemia during aortic clamping, haemodynamic instability, ischaemiaereperfusion injury, and reduced intercostal and lumbar perfusion. To reduce the incidence of spinal cord ischaemia, surgical techniques have evolved to combat each of these pathological mechanisms. Open repair of TAAA is now commonly performed on left heart bypass with distal aortic perfusion, sequential aortic clamping, intercostal reimplantation, visceral perfusion, cerebrospinal fluid (CSF) drainage, and the utilisation of evoked potential monitoring to guide surgical strategies. 1 However, the advent of endovascular repair of TAAA has posed a different set of challenges. While spinal cord injury remains a significant complication, 2 the pathogenesis has not been so extensively studied, and strategies to reduce the incidence of neurological complications are still being formulated. Fundamentally, spinal cord ischaemia after endovascular repair of TAAA appears to be primarily caused by coverage of the thoracoabdominal aorta with an endograft that reduces or abolishes flow through the intercostal and lumbar arteries. Therefore, the causative mechanism would appear to be primarily ischaemic, although embolisation has been implicated in some cases of immediate postoperative paraplegia. As a consequence, endovascular strategies have evolved in an attempt to reduce spinal cord injury, although there is no absolute consensus around a “gold standard” set of procedural and adjunctive preventive measures. The primary management strategy for preventing and treating spinal cord ischaemia is achieving an effective spinal cord perfusion pressure. The principle determinants of spinal cord perfusion pressure are the mean arterial pressure (MAP) and CSF pressure. Most experts would agree than an effective MAP is essential to prevent spinal cord ischaemia. The place of CSF drainage (whether routine or selective) is more controversial, although it appears to be of benefit in symptomatic patients, and has become extensively utilised. In light of the ischaemic aetiology of spinal cord injury, maintenance of existing collateral perfusion to the spinal cord would appear to be important in preventing neurological complications. The spinal cord vascular plexus receives important contributions from the vertebral and hypogastric arteries, and maintaining perfusion through these vascular beds is likely to influence favourably spinal cord perfusion. 3 Recently, several authors have suggested that staging endovascular TAAA procedures may deliver benefits regarding the prevention of spinal cord ischaemia. Staging these procedures maintains a degree of aneurysm sac perfusion through not attempting to obtain complete aneurysm exclusion during the primary procedure. Staging may be achieved in one of several ways, including staging the thoracic and abdominal components; leaving an anatomical branch unstented (e.g., coeliac or iliac); or incorporating a dedicated perfusion branch. In between the procedural stages, the spinal cord is theoretically exposed to a relative degree of ischaemia, which may then stimulate collateral formation. 4 The endovascular reconstruction may then be completed at a later date. The second procedure is usually of a smaller magnitude than the primary procedure and may be performed under local anaesthesia with evoked potential monitoring. In the preceding article, Kasprczak et al. 5 describe their

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