Control of proximal hypertension during aortic cross-clamping: its effect on cerebrospinal fluid dynamics and spinal cord perfusion pressure

Abstract

Postoperative paraplegia remains the most devastating complication of surgery of the descending and thoraco-abdominal aorta. Control of the proximal hypertension that follows cross-clamping of the thoracic aorta to repain aneurysms of the descending and thoraco-abdominal aorta is necessary to prevent left ventricular failure, myocardial infarction, and hemorrhagic cerebral events. Both pharmacological and mechanical modalities used to control central hypertension during aortic occlusion affect cerebrospinal fluid dynamics and spinal cord perfusion pressure. Sodium nitroprusside (doses >5 microg/kg/min), the most widely used pharmacological agent, decreases spinal cord perfusion pressure because it increases cerebrospinal fluid pressure and decreases blood pressure distal to the aortic cross-clamp. This effect cannot be prevented by drainage of cerebrospinal fluid. Nitroglycerin also decreases spinal cord perfusion pressure, but its effects on cerebrospinal fluid dynamics can be countered by drainage of cerebrospinal fluid. Active distal perfusion with left atrial-femoral artery bypass can provide adequate perfusion of the circulation distal to the aortic cross-clamp while simultaneously reducing cerebrospinal fluid pressure. This approach can maintain mesenteric and spinal cord blood flow, therefore preventing the multiple organ dysfunction syndrome caused by release of cytokines from the splanchnic district and decreasing the incidence of postoperative paraplegia from spinal cord ischemia. In cases of limited retroperfusion, partial exsanguination and cerebrospinal fluid drainage can be used in conjunction with left atrial-femoral artery bypass to prevent rises in cerebrospinal fluid pressure and maintain spinal cord blood flow above the threshold necessary to prevent neurological injury. The use of oxygenated perfluorocarbons in the subarachnoid space to provide passive oxygenation of the spinal cord during aortic occlusion remains experimental and requires further investigation.