Abstract

URING THE PAST 20 years, major advances in the intraoperative management of patients undergoing thoracoabdominal aortic aneurysm (TAAA) surgery have substantially reduced postoperative primary morbidity and mortality. At present, mortality rates after TAAA repair are estimated to be 5% to 10%, neurologic deficits 3% to 10%, renal failure 8% to 29%, and pulmonary complications 30% to 40%.1-4 Among the most feared complications of thoracic aortic aneurysm (TAA) and TAAA surgery are paraparesis and paraplegia, which are estimated to occur in 6% to 10% of patients who undergo TAA or TAAA repair. 5,6 Patients with these complications have a 20% greater risk of mortality than do patients without postoperative paraparesis or paraplegia. These patients, who are usually older, require intensive rehabilitation. A patient’s risk of postoperative paraparesis and paraplegia is determined by aneurysmal extent, acute dissection, cross-clamp time, preoperative renal dysfunction, previous aortic surgery, diabetes, and rupture.7 Improvements in TAAA repair procedures, including reduced cross-clamp time, distal aortic perfusion, and reattachment of intercostal arteries, have minimized critical ischemic times. Adjuncts such as cerebrospinal fluid (CSF) drainage, spinal cord monitoring, atrial femoral bypass, regional and systemic cooling, intrathecal papaverine, intraoperative use of naloxone, steroids and barbiturates, and the recognition and treatment of factors related to coagulopathy, have also been introduced. 8 The arterial circulation of the spinal cord consists of 2 interconnected sources: intrinsic and extrinsic. The intrinsic blood supply consists of a single anterior spinal artery (ASA), which courses along the ventral aspect of the cord and ultimately supplies the bulk of the cord substance through penetrating arteries, and paired posterior spinal arteries, which supply the remainder of the cord. This intrinsic circulation in turn receives its extrinsic blood supply via the radiculomedullary arteries, although the anatomic details of this supply vary among individuals. The principal extrinsic blood supply in the cervical and upper thoracic region comes from branches of the vertebral arteries; the thoracolumbar cord is supplied by intercostal and lumbar arteries, and the conus is supplied by the lateral sacral branches of the hypogastric vessels. There are 2 aspects of the spinal cord circulation that explain the risk of cord ischemia during TAAA repair. First, the diameter and continuity of the ASA vary along its length. Angiographic studies have shown that the ASA becomes extremely narrow cephalad to its anastomosis with the great radicular artery. Second, the human spinal cord is irregularly supplied by the radiculomedullary arteries because only few of them actually reach the cord substance. The thoracolumbar region is at the most risk for ischemic injury because this region is typically supplied by a single radiculomedullary artery, better known as the artery of Adamkiewicz or arteria radicularis magna. This artery has been shown to arise from T9 to T12 in about 75% of individuals. Because this area falls within the segment of the aorta that is clamped during reconstruction, clamping can compromise the blood supply to the cord. With proximal descending aortic cross-clamping, adequate spinal cord perfusion requires ASA patency, collateral circulation, and sufficient spinal cord perfusion pressure, defined as the difference between spinal artery pressure and CSF pressure. 9 During hypoxia and hypercarbia, autoregulation of spinal cord blood flow is lost and flow becomes linearly related to perfusion pressure. For this reason, adjuncts that decrease CSF pressure will increase spinal cord perfusion pressure. The rationale for using a CSF drain is based on experimental data showing that (1) CSF pressure increases during aortic clamping and (2) reducing CSF pressure improves spinal perfusion. Drenger et al 10 observed acute increases in CSF pressure immediately after applying the aortic clamp during TAAA repair. These increases were similar in patients with and without distal bypass and have been attributed to a sudden elevation of cerebral blood flow. The authors also observed a second peak

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