Intraoperative adjuncts of spinal cord protection

Abstract

Immediate neurological deficits as a complication of aortic surgery occur as the direct result of hypoxia, related to the acute deprivation of spinal cord blood supply inflicted by prolonged aortic cross-clamping (AXC). The etiology of spinal cord ischemia constitutes a series of progressive interdependent events which include proximal hypertension, increase in cerebrospinal fluid pressure, perioperative hypotension, inadequate perfusion to critical intercostal or lumbar vessels, extent of aortic pathology and duration of AXC. Several intraoperative interventions and strategies, which address the multifactorial nature of cord injury, are presented by the authors. Of critical importance is the role of adequate distal aortic perfusion, with either left atrium-femoral artery (LA-FA) bypass or arterial-arterial passive shunts, to control both central hypertension, through proximal unloading, and hypotension distal to AXC. Equally crucial is the increase in CSF pressure, secondary to proximal hypertension, which acts antagonistically to distal aortic pressure in regulating spinal cord perfusion pressure (SCPP). Cerebrospinal fluid drainage (CSFD) reduces CSF pressure to offset SCPP to favor cord perfusion. Pharmacological agents, such as papaverine and steroids in combination with CSFD, produce a synergistic benefit of extending the time interval of safe AXC. Encouraging results have also been realized with circulatory arrest and profound hypothermia which reduce oxygen demand of neural tissues and extend the safe duration of AXC interval. The use of distal bypass is most effective with CSFD as an integral component of a multimodality approach, which also incorporates the intraoperative monitoring of somatosensory evoked potentials (SSEP), to detect the onset of spinal cord ischemia and assess the adequacy of distal aortic perfusion and disposition of critical segmental vessels.