Annals of Vascular Surgery
Volume 20, Issue 2 , Pages 188-194, March 2006

Endovascular Thoracic Aortic Repair and Previous or Concomitant Abdominal Aortic Repair: Is the Increased Risk of Spinal Cord Ischemia Real?

Division of Vascular Surgery, Department of Surgery, Mount Sinai School of Medicine, New York, NY, USA

Article Outline

Spinal cord ischemia after endovascular thoracic aortic repair remains a significant risk. Previous or concomitant abdominal aortic repair may increase this risk. This investigation reviews the occurrence of spinal cord ischemia after endovascular repair of the descending thoracic aorta in patients with previous or concomitant abdominal aortic repair. Over an 8-year period, 125 patients underwent endovascular exclusion of the thoracic aorta at the Mount Sinai Medical Center. Twenty-eight of these patients had previous or concomitant abdominal aortic repair. The 27 patients who underwent staged repairs all had cerebrospinal fluid (CSF) drainage during and following repair. This population was analyzed for the complication of spinal cord ischemia and factors related to its occurrence. Mean follow-up was 19.3 months (range 1–61). Spinal cord ischemia developed in four of the 28 patients (14.3%) who underwent endovascular thoracic aortic repair with previous or concomitant abdominal aortic repair, while one of 97 patients (1.0%) developed ischemia among the remaining thoracic endograft population. One patient with concomitant abdominal aortic repair developed cord ischemia that manifested 12 hr following the procedure. The remaining three patients with previous abdominal aortic repair developed more delayed-onset paralysis ranging from the third postoperative day to 7 weeks following repair. Irreversible cord ischemia occurred in three patients, with full recovery in one patient. Major complications from CSF drainage occurred in one patient (3.7%). Spinal cord ischemia occurred at a markedly higher rate in patients with previous or concomitant abdominal aortic repair. This risk continued beyond the immediate postoperative period. The benefit of perioperative and salvage CSF drainage remains to be determined.

 

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INTRODUCTION 

Spinal cord ischemia following endovascular thoracic aortic repair occurs in 0–12% of patients.1, 2, 3, 4, 5, 6, 7, 8, 9 The etiology of spinal cord ischemia appears to be multifactorial.10, 11, 12 One proposed risk factor for spinal cord ischemia following endovascular thoracic aortic repair is previous abdominal aortic surgery.4, 13 Twenty-five percent of patients with thoracic aortic aneurysms (TAAs) have concomitant abdominal aortic aneurysms (AAAs).14 Given the risk of rupture, surgical repair has been advised for both of these entities. However, the risk of spinal cord ischemia in this group of patients requiring multiple aortic operations has not been fully elucidated.

In this study, we reviewed our experience with endovascular thoracic aortic repair in patients who underwent previous or concomitant abdominal aortic repair to determine the risk of spinal cord ischemia in this patient group and to possibly identify any inciting factors.

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METHODS 

Since 1997, 125 patients have undergone endovascular thoracic aortic repair at our institution. Of these, 27 underwent endovascular TAA repair following either conventional or endovascular AAA repair. A single patient underwent simultaneous endovascular TAA repair and conventional AAA repair. All patients were treated in accordance with the institutional review board of the Mount Sinai Medical Center.

Preoperative computed tomography (CT) and angiography were performed in all patients to determine aortic anatomy for endograft sizing. Locations of patent intercostal arteries in relation to the aneurysm and the landing zones were noted. However, selective intercostal artery angiography was not performed. All procedures were performed in the operating room with portable C-arm fluoroscopy. All patients who underwent staged repairs had cerebrospinal fluid (CSF) drainage catheters placed preoperatively before their endovascular TAA repairs. Access to the thoracic aorta was via the femoral or iliac artery. Endografts used included the Talent (Medtronic, Minneapolis, MN), TAG Excluder (W. L. Gore, Flagstaff, AZ), and the Relay (Bolton Medical, Sunrise, FL).

Follow-up included an office visit with the operating surgeon in addition to anteroposterior and lateral abdominal radiographs and contrastenhanced CT angiograms at 1, 6, and 12 months after hospital discharge and annually thereafter (Fig. 1).

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RESULTS 

Of the 28 patients who underwent endovascular TAA repair simultaneously or following previous AAA repair, four (14.3%) developed neurological symptoms attributable to spinal cord ischemia. Conversely, only one of 97 patients (1.0%) who underwent endovascular TAA repair without a history of previous or concomitant AAA repair developed spinal cord ischemia. The overall rate of paraplegia for the entire patient group undergoing endovascular TAA repair was therefore 4%. Of the patients with previous AAA repair who developed paraplegia, one developed symptoms during the first postoperative night after initially having an intact neurological exam upon awaking from anesthesia. The other three patients had more delayed onset of their symptoms, all following initial hospital discharge, ranging from 3 days to 7 weeks postoperatively.

Clinical summaries for these patients are as follows (Table I).

Table I. Clinical summary of patients
PatientAneurysm length (mm)Distance from distal graft to celiac axis (mm)Status of hypogastrics at time of thoracic repairPerioperative hypotensionTime until neurological deficitNeurological outcome
12759Patent bilaterallyNo2 daysParalysis
216012Patent bilaterallyYes12 hrComplete resolution
323514Patent bilaterallyNo4 weeksParalysis
428526Patent bilaterallyNo7 weeksParalysis

Patient 1 underwent successful elective endovascular exclusion of his descending thoracic aneurysm. He had undergone conventional AAA repair 6 years prior. The stent graft extended from just distal to the left subclavian artery to immediately proximal to the celiac axis. He was discharged home on postoperative day 1 with normal neurological function. On postoperative day 3, he experienced sudden lower extremity paralysis. Magnetic resonance imaging (MRI) revealed spinal cord infarction from the T10 level to the conus. The patient failed to recover neurological function.

Patient 2 had successful deployment of the first of two thoracic aortic endograft devices measured for elective exclusion of her TAA. Maldeployment of the second device across the visceral segment of the abdominal aorta necessitated transabdominal exposure of the infrarenal aorta and extraction of the misdeployed endograft. The infrarenal abdominal aorta was aneurysmal, measuring 4 cm in diameter; therefore, an infrarenal tube graft repair was performed. TAA exclusion was completed via a side-arm limb sewn to the tube graft. The patient's overnight hospital course was remarkable for two periods of hypotension (systolic blood pressure to 90 mm Hg), which responded to fluid resuscitation. She was noted to have left leg paralysis and right leg weakness on postoperative day 1. CSF drainage was placed immediately. Steroids were administered, and her blood pressure was supported with intravenous fluids. MRI noted an unremarkable spinal cord signal. Dramatic improvement in the neurological deficit was seen in the first 12 hr, followed by complete resolution. She remained free of any neurological deficit over a 38-month follow-up.

Patient 3 underwent successful elective endovascular exclusion of his descending thoracic aneurysm. He had undergone conventional AAA repair 3 years prior. The stent graft extended from the left subclavian artery to the midthoracic aorta. He was discharged home on postoperative day 2, neurologically intact. The patient presented 4 weeks later with 2 days of bilateral leg weakness. MRI revealed no evidence of spinal cord infarction. His symptoms improved in the initial hours following admission. Electromyography showed an L1-level radicular dysfunction, suggestive of ischemic anterior horn cells, and the neurology consultant's diagnosis was spinal cord ischemia without infarct. By hospital day 4, the patient markedly improved and was discharged. Six weeks later, he presented to the emergency department, having experienced 3 days of progressive lower extremity weakness, culminating in incontinence, then paralysis. A CSF drain was placed, and steroids were administered but with no effect. The patient has remained paraplegic.

Patient 4 underwent successful endovascular exclusion of his thoracic aneurysm. He had undergone conventional AAA repair 4 years prior. The patient returned to the hospital 7 weeks following his discharge, complaining of right lower extremity weakness. Neurology consultation was obtained; a T6 Brown-Sequard lesion was diagnosed clinically, and a spinal cord infarction was confirmed on MRI. At the time of diagnosis, a CSF drain was placed and steroids were administered. The patient regained significant function of his extremity and was discharged to a rehabilitation facility. He returned to the hospital 2 weeks later with complete paralysis of his right lower extremity. MRI at that time showed the same infarction seen previously as well as central and anterior cord infarction just above the level of T5. He failed to regain any neurological function.

During the same time period that was reviewed, of patients without a previous or concomitant AAA repair who underwent endovascular TAA repair, only one experienced spinal cord ischemia. Additionally, over the same time period, there were eight patients who had endovascular TAA repairs and went on to have AAA repairs, seven of which were endovascular. Also, there were 12 patients who underwent endovascular AAA repair following open TAA repair. CSF drainage was implemented for all of these patients at the time of their AAA repair. There were no neurological complications in these groups.

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DISCUSSION 

Paraplegia following endovascular TAA repair occurs in a reported 0–12% of patients.1, 2, 3, 4, 5, 6, 7, 8, 9 Several recent large trials have reported paraplegia rates at the lower, but still significant, end of this range with the Gore TAG device (3%),8 the Talent device (4.3%),3 and the Zenith (Cook, Bloomington, IL) TX1 and TX2 devices (2%).6 Previous or simultaneous AAA repair has been postulated to be a risk factor for spinal cord ischemia and subsequent neurological insult following endovascular TAA repair.3, 4, 8, 13 A reported 25% of patients with a TAA have a concomitant AAA.14 Given this incidence and the risk of spinal cord ischemia, the management of these patients is evolving at the present time along with the development of new endovascular devices and methods of spinal cord protection. Although there are reports of successful simultaneous repairs using exclusively conventional open repair,15 endovascular techniques,16 or a combination of conventional AAA repair with endovascular TAA repair,17 the risk of spinal cord ischemia remains a major concern following such complex procedures. Additionally, with a mortality of up to 11%,15 staged repair appears to be a safer approach.

Endovascular repair of thoracic aortic disease offers several theoretical advantages over conventional repair with regard to the risk of spinal cord ischemia. With endovascular repair, there is no aortic occlusion, thereby avoiding much of the proximal hypertension which leads to autoregulatory disturbances in cerebral perfusion pressure. Additionally, perfusion of the spinal cord via distal aortic branches is maintained throughout the procedure. Furthermore, without aortic occlusion, reperfusion of the spinal cord and its associated release of inflammatory mediators is minimized. Despite these conceptual physiological advantages, spinal cord ischemia continues to occur following endovascular TAA repair at rates comparable to open repair. One factor that may be contributory to this is that endovascular repair does not allow for intercostal reimplantation at the time of operation. Sacrificing a greater number of intercostals (>10) has been associated with a higher incidence of paralysis in open repair of thoracic and thoracoabdominal aneurysms.18 Furthermore, intercostal reimplantation in open thoracoabdominal repair of the T9 and T10 arteries is associated with a lower risk of late neurological deficit.19 For these reasons, the location of intercostals should be noted preoperatively and spared when feasible while still allowing for an adequate landing zone.

Similar to spinal cord ischemia following open TAA repair, the etiology following endovascular repair is thought to be multifactorial.10 Spinal cord ischemia may occur immediately following stent graft deployment as a result of occlusion of vital intercostal arteries. Arterial occlusion may occur by direct coverage of the arterial orifice or via atheroembolization. Atheroembolization is known to occur during endovascular repair, often as a result of catheter manipulation, and may disseminate emboli to the arterial branches supplying the pelvis, lower extremities, and spinal cord. Furthermore, spinal cord ischemia may occur in a delayed fashion following stent graft deployment when a patient develops hypotension leading to subsequent loss of collaterals that were maintaining an adequate blood supply to the spinal cord despite intercostal interruption. Additionally, coverage of critical intercostal arteries may not lead to their immediate occlusion and flow may be maintained through cross-collateral flow, seen as endoleak on follow-up imaging. With sealing of these endoleaks, cross-collateral flow is lost as well, leading to subsequent intercostal occlusion. Two patients in our series had documented endoleaks on CT scans prior to their presentations with symptoms of spinal cord ischemia. Both of these patients went on to have spontaneous sealing of these endoleaks. Finally, despite incomplete aortic occlusion, there may still be some cytokine release associated with stent graft deployment and aortic manipulation that contributes to spinal cord ischemia.

In our experience, previous AAA repair appears to place patients undergoing endovascular TAA repair at high risk for spinal cord ischemia. Perhaps reduction in the number of collateral arteries supplying the spinal cord is the dominant factor. Of note, in our four patients, all internal iliac arteries were spared during AAA repairs, suggesting that patent lumbar arteries from the abdominal aorta are more contributory to spinal cord perfusion than iliolumbar branches.20 In our series, preoperative patency of the vertebral arteries was not recorded unless coverage of the left subclavian artery was anticipated. This is one limitation of the study given the contribution of collaterals from the vertebral arteries to the spinal cord. Nevertheless, the left subclavian artery was not covered in any of the four patients who developed spinal cord ischemia in our series. Additionally, greater length of aortic coverage appears to be a risk factor for the development of neurological symptoms following endovascular TAA repair,7, 8 presumably based on the same principle of coverage of lumbars and intercostals (Fig. 2). In our affected patient population, the length of preserved distal thoracic aorta proximal to the celiac axis ranged 9–26 mm. Furthermore, of the patients who developed paraplegia, three of four had the distal end of their grafts lie within 2 cm of the celiac axis, while only eight of the 24 unaffected patients had the distal end of their grafts within 2 cm of the celiac axis. Although these are small cohorts, it appears that if coverage to the level of the celiac axis is required for endovascular aneurysm exclusion, open repair may be warranted to allow for additional protective measures to limit the incidence of paraplegia.

  • View full-size image.
  • Fig. 2. 

    (a) MRI demonstrates an artery originating from a TAA which will be covered with a stent graft. (b) CT showing multiple levels of arterial blood supply to the spinal cord.

A wide variety of techniques have been utilized to prevent spinal cord ischemia during TAA repair. In conventional repair, these have included distal aortic perfusion, hypothermic circulatory arrest, local hypothermia, spinal cord monitoring, CSF drainage, strict blood pressure control, as well as the use of a number of pharmacological agents including steroids, naloxone, barbituates, and papaverine. With endovascular TAA repair, many of these techniques are not relevant. However, both strict perioperative blood pressure control and CSF drainage remain applicable.

Avoidance of hypotension following TAA repair helps to maintain blood flow to the spinal cord through what may be a marginal collateral supply. Perioperative hypotension has been shown to be a significant predictor of spinal cord ischemia following both endovascular TAA repair2 and conventional open TAA repair.21, 22 One patient in our series had documented postoperative hypotension that was managed with fluid resuscitation. The other three patients all presented after hospital discharge, making blood pressure monitoring impossible. It is difficult to know what, if any, role hypotension may have played in the late development of their neurological symptoms. However, this reinforces that perioperative hypotension should be aggressively avoided and may necessitate copious fluid resuscitation or even the use of vasopressors. Furthermore, this raises the issue that even postdischarge blood pressure should be maintained at normal or supranormal levels to lower the risk of delayed spinal cord ischemia.

CSF drainage during TAA repair is based on the principle that spinal cord perfusion may be increased by lowering the intrathecal pressure. The spinal cord is located within the bony confines of the spinal canal, and a small increase in the volume of the spinal cord in the form of spinal cord edema will lead to a rise in CSF pressure. This increased pressure limits blood flow to the spinal cord, which is simultaneously limited by the sacrificing of intercostal and lumbar arteries. CSF drainage relieves this pressure and is thought to enhance blood flow to the spinal cord. Both a meta-analysis23 and a randomized clinical trial24 have shown that CSF drainage lowers the incidence of neurological deficits following conventional TAA repair. Although its role in endovascular TAA repair has not been clearly defined in any large trials, our protocol is to implement CSF drainage for up to 48 hr in any patient undergoing endovascular TAA repair who has had previous abdominal aortic surgery. This was done for our three patients who underwent staged repairs, who all, unfortunately, still developed neurological deficits but in a delayed fashion.

Patients undergoing endovascular TAA repair who present with late neurological complications present a particular challenge. Institution of CSF drainage has been successful in reversing neurological deficits presenting early postoperatively (<24 hr) following endovascular TAA repair25, 26 as well as late postoperatively (14 days) following conventional TAA repair.27, 28 Of the three patients who presented more than 24 hr postoperatively with neurological deficits, two had CSF drains placed. One of these patients had significant improvement in his symptoms initially, while the other remained paraplegic. Despite these mixed results, CSF drainage along with the administration of steroids remain the primary salvage treatments, and we believe both should be performed in these patients. Also, the delayed development of neurological symptoms following endovascular TAA repair should alert the surgeon to assure that there has not been device migration and subsequent coverage of intercostal arteries. There was no evidence of device migration in the patients presented here.

Although both preoperative and delayed insertion of CSF drains appear to be beneficial in patients undergoing endovascular TAA repair following AAA repair, the procedure is not without its own inherent risks. In particular, subdural hematoma has been reported to occur at a rate of 3.5% following thoracoabdominal aortic aneurysm repair with CSF drainage, with an associated 67% mortality rate.29, 30 Furthermore, drain complications have been associated with a greater risk of neurological deficit.21 In our series, one patient developed a subarachnoid hemorrhage from a traumatic drain placement, which led to chemical meningitis, mental status changes, and subsequent aspiration requiring prolonged ventilatory support. Malfunctioning CSF drains should be either removed or replaced depending on the time course relative to the operation. In spite of the fact that patients may develop delayed spinal cord ischemia even with the use of perioperative CSF drainage, the data available seem to indicate that the benefits of CSF drainage outweigh the risk of complications.

Endovascular TAA repair can be performed with acceptable perioperative morbidity and mortality. However, there continues to be a low but significant incidence of spinal cord ischemia. This incidence is markedly increased in our experience in patients who had previous abdominal aortic surgery. Preventative measures including CSF drainage should be used for this subgroup of patients, although more experience is necessary to fully delineate the benefits. Furthermore, the risk of spinal cord ischemia in these patients is present not merely in the immediate postoperative period but continues to be a factor in the weeks after the operation. Patients presenting with late-onset spinal cord ischemia may benefit from CSF drainage and steroid administration. Despite the advancing technology of endovascular techniques, it is apparent that patients with coexisting thoracic and abdominal aortic disease will continue to present surgeons with therapeutic challenges to avoid the devastating complication of spinal cord ischemia.

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PII: S0890-5096(06)60030-7

doi:10.1007/s10016-006-9010-6

Annals of Vascular Surgery
Volume 20, Issue 2 , Pages 188-194, March 2006

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