The Annals of thoracic surgery
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Spinal cord injury following operations on the descending thoracic or thoracoabdominal aorta remains a major problem. In certain subsets of patients, the risk of postoperative spinal cord injury is substantial. Although several adjuncts have been employed clinically to eliminate or reduce the frequency of this complication, none have proven to be completely effective. ⋯ Since postoperative spinal cord injury most likely results from ischemia or hypoxia of the lower segment of spinal cord, use of adjunctive techniques to preserve spinal cord function during aortic clamping by perfusing the distal aorta adequately with or without systemic hypothermia should be considered. To practically implement this, partial cardiopulmonary bypass for distal perfusion when the critical intercostal or lumbar arteries originate from the aorta distal to the excluded segment, and total cardiopulmonary bypass with systemic hypothermia and implantation of intercostal and lumbar arteries when these arteries originate from the excluded segment, can be used. In addition, whenever possible, intraoperative monitoring of spinal cord function should be performed.
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Comparative Study Clinical Trial Controlled Clinical Trial
Effects of aprotinin on hemostatic mechanisms during cardiopulmonary bypass.
Cardiopulmonary bypass (CPB) is associated with activation of humoral systems, which results in the release of proteases. These proteases may affect platelets and stimulate granulocytes. In the present study, the protease inhibitor aprotinin was given in high doses to 11 patients to achieve plasma concentrations of more than 150 kallikrein inactivator units per milliliter during CPB. ⋯ Postoperatively, hemostasis was significantly better preserved after aprotinin treatment (blood loss of 357 ml in the treated group versus 674 ml in the untreated group; p less than 0.01). Since tissue-plasminogen activator activity was similar in both groups, the improved hemostasis most likely should be attributed to platelet preservation. Furthermore, aprotinin lessened neutrophilic elastase release, which might contribute to decreased pulmonary dysfunction in patients at risk.