Robertazzi R R, Cunningham J N
Department of Surgery, Maimonides Medical Center, Brooklyn, NY 11219, USA.
Semin Thorac Cardiovasc Surg. 1998 Jan;10(1):29-34. doi: 10.1016/s1043-0679(98)70014-0.
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.
作为主动脉手术并发症的即刻神经功能缺损，是由于缺氧直接导致的，而缺氧与长时间主动脉交叉阻断（AXC）造成的脊髓血供急性剥夺有关。脊髓缺血的病因构成了一系列渐进的相互依存事件，包括近端高血压、脑脊液压力升高、围手术期低血压、关键肋间或腰血管灌注不足、主动脉病变程度以及AXC持续时间。作者介绍了几种针对脊髓损伤多因素性质的术中干预措施和策略。至关重要的是充分的远端主动脉灌注的作用，可通过左心房-股动脉（LA-FA）旁路或动脉-动脉被动分流来实现，以通过近端卸载控制中心高血压，并控制AXC远端的低血压。同样关键的是，继发于近端高血压的脑脊液压力升高，在调节脊髓灌注压（SCPP）时与远端主动脉压力起拮抗作用。脑脊液引流（CSFD）可降低脑脊液压力以抵消SCPP，从而有利于脊髓灌注。诸如罂粟碱和类固醇等药物与CSFD联合使用，可产生协同效益，延长安全AXC的时间间隔。循环停止和深度低温也取得了令人鼓舞的结果，这可降低神经组织的氧需求并延长AXC间隔的安全持续时间。将远端旁路与CSFD结合使用最为有效，CSFD是多模式方法的一个组成部分，该方法还包括术中体感诱发电位（SSEP）监测，以检测脊髓缺血的发生，并评估远端主动脉灌注的充分性以及关键节段血管的分布情况。
