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Low incidence of paraplegia after thoracic endovascular aneurysm repair with proactive spinal cord protective protocols
From the Midwestern Vascular Surgical Society
Low incidence of paraplegia after thoracic endovascular aneurysm repair with proactive spinal cord protective protocols Joseph L. Bobadilla, MD,a Martha Wynn, MD,b Girma Tefera, MD,c and C. W. Acher, MD,c Lexington, Ky; and Madison, Wisc Objective: Paraparesis and paraplegia after thoracic endovascular aneurysm repair (TEVAR) is a greatly feared complication. Multiple case series report this risk up to 13% with no, or inconsistent, application of interventions to enhance and protect spinal cord perfusion. In this study, we report our single-institution experience of TEVAR, using the same proactive spinal cord ischemia protection protocol we use for open repair. Methods: Endovascular thoracic aortic interventions were performed for both on-label (aneurysm) and off-label (trauma, other) indications. Aortic area covered was recorded as a fraction from the subclavian to celiac origins and reported as a percentage. If debranching was required, measurements were taken from the most distal arch vessel left intact. Intraoperative imaging and postoperative computed tomographic angiogram were used in calculating aortic percent coverage. Outcomes were recorded in a clinical database and analyzed retrospectively. The spinal cord ischemia protection included routine spinal drainage (spinal fluid pressure <10 mm Hg), endorphin receptor blockade (naloxone infusion), moderate intraoperative hypothermia (<35 C), hypotension avoidance (mean arterial pressure >90 mm Hg), and optimizing cardiac function. Results: From 2005 to 2012, 94 consecutive TEVARs were studied. Indications were thoracic aneurysm (n [ 48), plaque rupture with or without dissection (n [ 23), trauma (n [ 15), and other (n [ 8). Forty-nine percent were acute, average age was 68.5 years, 60% (n [ 56) were male, and the mean follow-up was 12 months. Mean length of aortic coverage was 161 mm, correlating to 59.4% aortic coverage. One patient had delayed paralysis (1.1%; observed/expected ratio, 0.12) and recovered enough to ambulate easily without assistance. Other complications included wound (7.5%), stroke (4.3%), myocardial infarct (4.3%), and renal failure (1.1%). Conclusions: Proactive spinal cord protective protocols appear to reduce the incidence of spinal ischemia after TEVAR compared with historical series. This study would suggest that active, as opposed to reactive, approaches to spinal ischemia portend a better long-term outcome. Multimodal protection is essential, especially if long segment coverage is planned. (J Vasc Surg 2013;57:1537-42.)
Over the last 3 decades, great progress has occurred in reducing the incidence of spinal cord ischemia and paralysis after open thoracic aortic aneurysm repair.1,2 From the initial observation of the artery of Adamkiewicz nearly 150 years ago, to its implication in neurologic complications after aortic surgery over the past 50 years,3 to a more complex understanding of the collateral network concept,4 the rate of paraplegia after thoracic aortic surgery has declined slowly over time.1 It has been shown in open From the Department of Surgery, Vascular and Endovascular Surgery, University of Kentucky, Lexingtona; and the Department of Anesthesiologyb and Department of Surgery, Division of Vascular Surgery,c School of Medicine and Public Health, University of Wisconsin, Madison. Author conflict of interest: none. Presented in Poster Form at the Thirty-sixth Annual Meeting of the Midwestern Vascular Surgical Society, Milwaukee, Wisc, September 6-8, 2012. Reprint requests: Joseph L. Bobadilla, MD, Department of Surgery, University of Kentucky, 800 Rose St, Room C219 Lexington, KY 40536-0293 (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest. 0741-5214/$36.00 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery. http://dx.doi.org/10.1016/j.jvs.2012.12.032
aneurysm repair that multimodal protocols to protect and augment spinal perfusion are essential in reducing the incidence of this disabling complication.1,2,5-11 Furthermore, consistent and uniform application of these protocols is essential, as demonstrated by Hollier et al, where spinal ischemia was reduced from 6% to 0% over an 11-year period with the implementation of a proactive protocol.12 As the application of endovascular aneurysm repair has progressed to include thoracic pathologies, these theories again need to be revisited. Over the last decade, it has become increasingly apparent that thoracic endovascular aneurysm repair (TEVAR) carries the same risk of paraparesis/paraplegia as open thoracic aortic repair.13-17 A recent review by Rizvi and Sullivan estimated the overall risk of paraplegia/paraparesis after TEVAR to be 3.9%. This was based on a meta-analysis of 5349 patients in over 50 published reports. More importantly, the rate of paraplegia ranged from 0% to 13.3% among the reported case series, each with variable spinal cord protection protocols and inconsistent implementation.16 It is clear that with inconsistent application of interventions to enhance and protect spinal cord perfusion, paraplegia rates can be unnecessarily and unacceptably high.12,16 We have previously shown that aggressive spinal 1537
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fluid drainage is effective in reducing spinal cord ischemia, with an acceptable risk profile.18 The goals of any effective spinal protection protocol include increasing the spinal perfusion pressure, buffering the ischemia-reperfusion injury, and reducing the spinal cord metabolic demand. Specific interventions, either chemical or mechanical, addressing each of these fundamental points synergistically increase perfusion while reducing the ischemia/reperfusion response, neuronal metabolic activity, and excitotoxicity. In this study, we report our single-institution experience of TEVAR, using the same proactive spinal cord ischemia protection protocol we use for open aneurysm repair. This protocol consists of uniform spinal fluid drainage, permissive mild hypothermia, increasing mean arterial blood pressure, and multimodal pharmico-prophylaxis. METHODS During a 7-year contiguous period from January 1, 2005 to January 31, 2012, all TEVARs were prospectively enrolled into our institutional clinical database. Demographic data, clinical comorbidities, and outcomes data were recorded. In addition, postoperative complications including endoleak, wound-related complications, stroke, myocardial infarction, renal failure, paraplegia/paraparesis, and death were also monitored and recorded. All patients receiving a Food and Drug Administrationapproved thoracic endovascular device were included in analysis, regardless of on- or off-label indication for implantation. Both elective and emergent presentations were included in this cohort, as well as patients requiring either abdominal or cervical arch debranching procedures to ensure proper landing zone. Trauma patients with short segment coverage using extension cuff segments were excluded from this study. In standard TEVAR implantations, those patients not requiring a debranching procedure, aortic length covered was recorded, in centimeters, as a fraction from the left subclavian to celiac origins. Measurements were taken utilizing the intraoperative imaging and first postoperative computed tomographic angiogram scan. If either abdominal or arch debranching procedures were required to assure adequate landing zone, measurements were taken from the most distal arch vessel left intact to the most proximal abdominal branch vessel left intact. Because of the confounding issue of differing absolute aortic lengths among patients, the length of aortic coverage was normalized by calculating a percent aortic coverage. These calculations were completed retrospectively. Total aortic graft coverage length was divided by the total aortic length, allowing for better comparison of normalized percent aorta covered among patients with variable absolute lengths covered. The spinal cord ischemia protection protocol included routine spinal drainage in all patients. Spinal drains were placed in all patients, regardless of elective or emergent presentation, so long as hemodynamic stability allowed. In the setting of unstable rupture, operative intervention without spinal drainage can be undertaken, but we strive
to obtain spinal drainage in all patients. All patients in this cohort received spinal drains, which were placed in the operating room by our dedicated cardiovascular anesthesiology group. Goals of drainage were to a spinal fluid pressure 8 mm Hg intraoperatively and 10 mm Hg postoperatively. This was accomplished by draining in 5 to 15 mL aliquots utilizing a buretrol system until the target pressure was achieved. All drainage was accomplished by gravity alone. There was no volume limit threshold at which spinal fluid drainage was ceased, although average intraoperative volumes ranged from 100 to 130 mL. If bloody fluid drainage was noted, the spinal drain was clamped, and a stat noncontrast head computed tomography was obtained to evaluate for extra-axial hemorrhage. In uncomplicated cases, spinal fluid drainage was stopped and the spinal drain clamped once brisk lower extremity leg lifting was reproducibly present on physical examination. Spinal drains were routinely removed 24 to 48 hours after surgery. All patients received methylprednisolone 30 mg/kg after anesthetic induction, up to a maximum dose of 2 g. Patients also received mannitol, 12.5 g shortly after anesthesia induction. Mannitol has been shown to reduce cerebrospinal fluid pressures experimentally and clinically. Experimentally, mannitol has also been shown to function as a free-radical scavenger and serve as an osmotic diuretic with renal protective properties.19 Moderate intraoperative hypothermia was allowed through radiative loss and the administration of cold intravenous fluids, to a goal temperature of less than 35 C, but more than 32 C. Postoperatively, active rewarming (thermal warming blankets) was strictly avoided, only ambient rewarming was allowed. Active rewarming blankets were avoided because of the potential induction of peripheral vasodilation. This can result in shunting of blood away from central structures, including the spinal cord. Reduced blood flow coupled with increased temperature and metabolic demands are major contributors to spinal ischemia risk. During both the intraoperative and postoperative time frames, mean arterial blood pressures were kept >85 mm Hg. In addition, patients were maintained on a continuous naloxone infusion starting before anesthesia induction and lasting for 24 hours postoperatively. Naloxone infusion was prepared with 2.5 mg in 250 mL diluent (10 mcg/mL) and infused at 1 mcg/kg/h. RESULTS From 2005 to 2012, 94 consecutive TEVAR implantations were studied. All procedures were performed at a single institution. Indications for repair included degenerative thoracic aneurysm (n ¼ 48), plaque rupture/intramural hematoma (n ¼ 23), trauma (n ¼ 15), and other (n ¼ 8). The other group included acute type B dissection (n ¼ 3), pseudoaneurysm (n ¼ 4), and one patient with presumed aortoesophageal bleeding. There were no patients with known connective tissue disorders included in this study cohort. The mean aortic diameter at the time of intervention for those patients with a degenerative aneurysm was 6.5 cm (minimum, 5.6 cm; maximum,
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9.0 cm). Plaque rupture was defined as new evidence of ulcerated plaque or intramural hematoma with symptoms, including back or chest pain. All trauma patients with evidence of intimal disruption, intramural hematoma, or extravasation were considered for TEVAR. Indication for TEVAR in acute type B dissection included renovisceral or limb malperfusion. The mean follow-up time period was just over 12 months. Debranching procedures were required in 17 cases (18.1%); of these, 15 were arch debranchings and two abdominal debranchings. Any patient requiring extension of the proximal landing zone underwent debranching at the time of TEVAR, or in a staged procedure prior to TEVAR. All patients underwent prophylactic debranching preceding TEVAR. There were 14 subclavian transposition/bypass procedures completed. One patient underwent both left subclavian and left common carotid revascularization in preparation for TEVAR. Both abdominal debranching procedures consisted of four-vessel revascularization: celiac/hepatic, superior mesenteric artery, and both renal arteries. Comorbidities of the group are listed in Table I. The mean length of aortic coverage was 161 mm, and the average normalized aortic percent coverage was 59.4% of total aortic length. There were 10 endoleaks identified during the course of the study. Seven of these were either type Ia or Ib leaks; these were all treated with proximal or distal extension. There was one type III leak treated with a bridging device, and two type II leaks with no sac expansion that ultimately thrombosed on their own. There were no cases of paraplegia or paralysis related to the repeat interventions. There was one patient who developed a cold leg after percutaneous closure device failure resulted in common femoral artery occlusion. This was removed operatively with no long-term adverse sequaelae. In addition, seven (7.4%) patients developed wound breakdown or superficial wound infections. There were four patients each who suffered perioperative myocardial infarction or cerebrovascular accident (Table II). There was one delayed paralysis (1.1%; observed/ expected ratio, 0.12). This patient had undergone elective TEVAR covering the proximal 63% of the native aorta along with arch debranching with a subclavian transposition for aneurysmal disease, patient number 37 (Fig). The paraplegia was associated with a period of postoperative hypotension. It responded to aggressive blood pressure augmentation and fluid resuscitation. The patient was able to recover and ambulate easily without assistive devices at the time of discharge. During the course of the study, there were no other patients that presented with delayed paraplegia. There were seven deaths during the course of this study. The mean time to death after TEVAR in these patients was 1.1 years (range, 0.72-1.86 years). Six of these were after hospital discharge and >30 days from the index case. There was one intraoperative death in this cohort. This was an 87-year-old female who presented with an acute plaque rupture and extensive intramural hematoma.
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Table I. Patient characteristics Category
Value (%)
Age, years Sex Male Female Presentation Elective Emergent Indication Thoracic aneurysm Plaque rupture/hematoma Trauma Other Procedure Standard TEVAR TEVAR þ arch debranching TEVAR þ abdominal debranching Comorbidities None Coronary artery disease Chronic obstructive pulmonary disease Diabetes Hypertension ASA score ASA 1 ASA 2 ASA 3 ASA 4 ASA 5 ASA 6
54 6 15 56 (60) 38 (40) 48 (51) 46 (49) 48 23 15 8
(51) (24) (16) (9)
77 (82) 15 (16) 2 (2) 14 30 20 2 75
(15) (32) (21) (2) (80)
0 4 36 46 8 0
(0) (4) (38) (49) (8) (0)
ASA, American Society of Anesthesiologists; TEVAR, thoracic endovascular aneurysm repair. Summary data of patient demographics, acuity of presentation, indication for operation, and comorbid conditions in all 94 TEVAR patients.
Table II. Patient data and outcomes Category
Value (%)
Mean aortic length coverage, mm Mean aortic coverage, % Complications Endoleak Wound breakdown/infection Stroke Myocardial infarct Acute renal failure Paraplegia Death
161 6 73 59.4 6 19 10 7 4 4 1 1 7
(10.6) (7.4) (4.3) (4.3) (1.1) (1.1) (7.4)
TEVAR, Thoracic endovascular aneurysm repair. Summary of mean aortic distance (mm) and percent aortic coverage along with postoperative outcomes data in all 94 TEVAR patients.
Upon device deployment, the patient became precipitously hypotensive. Repeat angiogram showed proximal conversion to free rupture into the left chest. A second device was brought on the field to deploy more proximally, but the patient ultimately expired in the operating room. There was one complication related to spinal drain placement in this patient group. This patient developed an epidural hematoma with cord compression after he was started on low-molecular-weight heparin. He had
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Fig. Percent aortic coverage. Each of the 94 patients in this study is represented by a single bar in this figure and numbered 1 to 94 accordingly. Patients are presented sorted by coverage extent and not chronological order for ease of interpretation. The open white bars represent proximal and/or distal uncovered aortic segments, measured as a percent of total aortic length. The blue shaded bar represents the percent of aorta covered with the thoracic endovascular aneurysm repair (TEVAR) devices. Patients requiring debranching procedures are noted by the blue (arch debranching) and purple (abdominal debranching) highlighted circles overlying the patient numbers. The solitary paraplegia patient, number 37, is also denoted with a red highlighted circle.
a history of aortic valve. He returned to our emergency room on postoperative day 6 with low back pain and bilateral lower extremity pain and weakness. Imaging revealed the epidural hematoma, and urgent decompressive laminectomy was completed. He regained function and recovered uneventfully. DISCUSSION In this study, we have examined the outcomes related to paraplegia and paraparesis after TEVAR with an aggressive and proactive spinal cord protection protocol. We observed an overall paraplegia event rate of 1.1%, much lower than other reported case series. In addition, this rate is lower than those results of the major multicenter international registry papers (European Collaborators on Stent Graft Techniques for Thoracic Aortic Aneurysm and Dissection Repair [EUROSTAR], 4.0%; GORE TAG
thoracic endoprosthesis registry [GORE-TAG], 3%; Talent Thoracic Retrospective Registry [TTR], 1.7%; Valiant Thoracic Stent Graft System Clinical Study [VALOR II], 2.5%).20-23 A recent meta-analysis review of published studies related to spinal protection showed an overall rate of paraplegia/paraparesis of 3.88%. Among those groups that employed routine spinal fluid drainage (SFD), this rate was 3.2%. Among those that never used SFD, the rate was 3.47%, and lastly, among those who selectively practiced SFD, the rate was 5.6%.24 Although our study is limited by the relatively low number of patients and heterogeneous pathologies, we believe it illustrates an essential concept about spinal cord perfusion and protection. Spinal cord perfusion during and after thoracic aortic surgery, including TEVAR, is maintained by a complex interplay between perfusion pressure, collateral networks, and the ischemia-reperfusion response. The ultimate goal
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of spinal cord protection must be the prevention of paraplegia/paraparesis using proactive measures and not rescue after it has already ensued. The consequences of failure to rescue are too great given the relatively simple and lowrisk prophylactic measures that can be implemented. In humans, the artery of Adamkiewicz has variable origin and is presumed to give rise to the greater radicular artery, a major feeder to the anterior spinal artery and perfusion source for the ventral motor columns.3 In addition, spinal cord blood flow is a plexus circulation with collateral feed from other intercostal radicular arteries, subclavian, vertebral, hypogastric, and other collateral contributors.25-27 When these collateral networks become compromised, or sacrificed, because of aortic surgery, spinal perfusion can suffer, and paraplegia may result.4 Certain patients are at increased risk for disruption of the plexus network. Those who have had prior aortic surgery, those with hypogastric or left subclavian stenosis/occlusion, and those with occluded lumbar arteries are at increased risk because of reduced inputs. In addition, those patients who require a long segment of thoracic coverage are at higher risk because of increased blood flow disruption. The more open intercostal arteries covered during TEVAR, the higher the risk of resulting paraplegia/paraparesis. It is because of the complex interplay of all these variables that spinal protection must be undertaken, especially in high-risk patients. Unfortunately, no single variable, or group of characteristics, can completely predict which patients will develop paraplegia/paraparesis post-TEVAR. Because of this, and the low morbidity associated with the interventions we utilize, we support the routine use of this proactive multimodal spinal protection in all patients undergoing formal TEVAR. The goals of spinal cord perfusion protection during thoracic aortic intervention are threefold: prolong spinal cord ischemic tolerance, reduce the ischemia reperfusion response, and improve spinal cord oxygen delivery. Improved ischemic tolerance can be accomplished with mild intraoperative hypothermia. We typically cool to 34 C. This helps to reduce spinal cord metabolic activity and spinal cord oxygen requirements. Ischemia-reperfusion injury can be attenuated with the routine use of induction steroid bolus to stabilize cellular membranes and minimize local inflammatory response pathways.28 In addition, naloxone infuse has been shown to reduce the release of excitatory neurotransmitters from ischemic neurons.29 Finally, mannitol acts as a free-radical scavenger, helping to blunt the reperfusion injury response.19 The third factor, spinal cord oxygen delivery, is the summation of hemodynamic and oxygen content factors. Blood flow is perhaps best visualized by the equation spinal cord perfusion pressure equals mean arterial blood pressure minus spinal fluid pressure. With this relationship, it is clear that augmentation of cardiac function and reduction in spinal fluid pressure are key to preserving spinal perfusion. We routinely employ spinal fluid drainage to augment microvascular perfusion. We choose an intraoperative drainage threshold of 8 mm Hg and
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a postoperative threshold of 10 mm Hg. This is in part because of our observations with open thoracic aortic surgery. We have noted a higher incidence of paraplegia/paraparesis in those patients with spinal fluid pressures over 10 mm Hg. Two recent studies have confirmed the observation that more aggressive spinal fluid drainage improves paraplegia/paraparesis rescue.30,31 The risks of spinal fluid drainage are low, and we believe are offset by the benefits derived from paraplegia prevention.18 We recommend holding prophylactic heparin dosing the morning of spinal drain removal and for the next 6 to 8 hours after drain removal. Obviously, adequate hemoglobin and oxygen are necessary to provide adequate tissue oxygen delivery, and avoidance of hypotension, hypoxemia, and anemia during and after intervention is essential. Oxygen delivery is directly dependent upon oxygen content, and we routinely strive for hemoglobin concentrations $10 g/dL. The use of active warming blankets can cause peripheral vasodilation, resulting in diversion of blood flow from central structures, including the spinal cord. For this reason, we advocate passive rewarming, which has the added benefit of maintaining reduced neuronal metabolic demands during this critical perioperative phase. When patients present with delayed paraplegia, we advocate the routine use of spinal fluid drainage and pharmacologic elevation of blood pressure to a mean pressure of 85 mm Hg or greater. Although endovascular thoracic aortic repair clearly provides an overall reduction in much of the morbidity associated with open thoracic aortic repair, paraplegia does not appear to be significantly reduced. TEVAR presents a unique insult to the spinal plexus network, with abrupt, oftentimes, long-segment input disruption and the added risk of embolization from lateral displacement of lining thrombus. In addition, this often occurs at relatively normothermic body temperatures, further amplifying the resulting ischemic injury. Because of this, we advocate a consistent approach to the prevention of paralysis/paraparesis during TEVAR based on the pathophysiology of spinal cord ischemia. We utilize the same multimodal protocol that is used during our open thoracic aneurysm repairs. Careful attention to cardiac function, perfusion pressure, spinal fluid pressure, along with chemoprophylaxis has reduced the incidence of spinal ischemia in our hands to roughly 1%, regardless of elective or emergent presentation. CONCLUSIONS Proactive spinal cord protective protocols appear to reduce the incidence of spinal ischemia after TEVAR when compared to historical series. This study would suggest that active, as opposed to reactive, approaches to spinal ischemia portend a better long-term outcome. The ultimate goal of spinal cord protection must be the prevention of paraplegia/paraparesis using proactive measures and not rescue after it has already occurred. The consequences of failure to rescue are too great given the relatively simple and low-risk prophylactic measures that can
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be implemented preemptively. Multimodal protection is essential, especially if long-segment coverage is planned. These strategies should include specific interventions directed toward improving spinal cord ischemic tolerance, reducing the ischemia reperfusion response, and improving spinal cord oxygen delivery. AUTHOR CONTRIBUTIONS Conception and design: JB, MW, GT, CA Analysis and interpretation: JB, MW, GT, CA Data collection: JB Writing the article: JB Critical revision of the article: JB, MW, GT, CA Final approval of the article: JB, MW, GT, CA Statistical analysis: JB, CA Obtained funding: Not applicable Overall responsibility: JB REFERENCES 1. Acher CW, Wynn M. A modern theory of paraplegia in the treatment of aneurysms of the thoracoabdominal aorta: an analysis of technique specific observed/expected ratios for paralysis. J Vasc Surg 2009;49: 1117-24; discussion: 1124. 2. Acher C, Wynn M. Outcomes in open repair of the thoracic and thoracoabdominal aorta. J Vasc Surg 2010;52:3S-9S. 3. Adams HD, Van Geertruyden HH. Neurologic complications of aortic surgery. Ann Surg 1956;144:574-610. 4. Griepp RB, Griepp EB. Spinal cord perfusion and protection during descending thoracic and thoracoabdominal aortic surgery: the collateral network concept. Ann Thorac Surg 2007;83:S865-9; discussion: S890-2. 5. Mell MW, Wynn MM, Reeder SB, Tefera G, Hoch JR, Acher CW. A new intercostal artery management strategy for thoracoabdominal aortic aneurysm repair. J Surg Res 2009;154:99-104. 6. Acher CW, Wynn MM, Mell MW, Tefera G, Hoch JR. A quantitative assessment of the impact of intercostal artery reimplantation on paralysis risk in thoracoabdominal aortic aneurysm repair. Ann Surg 2008;248:529-40. 7. Tefera G, Acher CW, Wynn MM. Clamp and sew techniques in thoracoabdominal aortic surgery using naloxone and CSF drainage. Semin Vasc Surg 2000;13:325-30. 8. Acher CW, Wynn MM, Hoch JR, Kranner PW. Cardiac function is a risk factor for paralysis in thoracoabdominal aortic replacement. J Vasc Surg 1998;27:821-8; discussion: 829-30. 9. Acher CW, Wynn MM. Multifactoral nature of spinal cord circulation. Seminars in thoracic and cardiovascular surgery 1998;10:7-10. 10. Acher CW, Wynn MM, Hoch JR, Popic P, Archibald J, Turnipseed WD. Combined use of cerebral spinal fluid drainage and naloxone reduces the risk of paraplegia in thoracoabdominal aneurysm repair. J Vasc Surg 1994;19:236-46; discussion: 247-8. 11. Acher CW, Wynn MM, Archibald J. Naloxone and spinal fluid drainage as adjuncts in the surgical treatment of thoracoabdominal and thoracic aneurysms. Surgery 1990;108:755-61; discussion: 761-2. 12. Hollier LH, Money SR, Naslund TC, Proctor CD Sr, Buhrman WC, Marino RJ, et al. Risk of spinal cord dysfunction in patients undergoing thoracoabdominal aortic replacement. Am J Surg 1992;164:210-3; discussion: 213-4. 13. Maeda T, Yoshitani K, Sato S, Matsuda H, Inatomi Y, Tomita Y, et al. Spinal cord ischemia after endovascular aortic repair versus open surgical repair for descending thoracic and thoracoabdominal aortic aneurism. J Anesth 2012:1-7.
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14. Ullery BW, Cheung AT, Fairman RM, Jackson BM, Woo EY, Bavaria J, et al. Risk factors, outcomes, and clinical manifestations of spinal cord ischemia following thoracic endovascular aortic repair. J Vasc Surg 2011;54:677-84. 15. Jonker FH, Verhagen HJ, Lin PH, Heijmen RH, Trimarchi S, Lee WA, et al. Open surgery versus endovascular repair of ruptured thoracic aortic aneurysms. J Vasc Surg 2011;53:1210-6. 16. Rizvi AZ, Sullivan TM. Incidence, prevention, and management in spinal cord protection during TEVAR. J Vasc Surg 2010;52:86S-90S. 17. Desai ND, Burtch K, Moser W, Moeller P, Szeto WY, Pochettino A, et al. Long-term comparison of thoracic endovascular aortic repair (TEVAR) to open surgery for the treatment of thoracic aortic aneurysms. J Thorac Cardiovasc Surg 2012;144:604-9; discussion: 609-11. 18. Wynn MM, Mell MW, Tefera G, Hoch JR, Acher CW. Complications of spinal fluid drainage in thoracoabdominal aortic aneurysm repair: a report of 486 patients treated from 1987 to 2008. J Vasc Surg 2009;49:29-34; discussion: 34-5. 19. Magovern GJ Jr, Bolling SF, Casale AS, Bulkley BH, Gardner TJ. The mechanism of mannitol in reducing ischemic injury: hyperosmolarity or hydroxyl scavenger? Circulation 1984;70:I91-5. 20. Leurs LJ, Bell R, Degrieck Y, Thomas S, Hobo R, Lundbom J, et al. Endovascular treatment of thoracic aortic diseases: combined experience from the EUROSTAR and United Kingdom Thoracic Endograft registries. J Vasc Surg 2004;40:670-9; discussion: 679-80. 21. Makaroun MS, Dillavou ED, Kee ST, Sicard G, Chaikof E, Bavaria J, et al. Endovascular treatment of thoracic aortic aneurysms: results of the phase II multicenter trial of the GORE TAG thoracic endoprosthesis. J Vasc Surg 2005;41:1-9. 22. Fattori R, Nienaber CA, Rousseau H, Beregi JP, Heijmen R, Grabenwoger M, et al. Results of endovascular repair of the thoracic aorta with the Talent thoracic stent graft: the Talent Thoracic Retrospective Registry. J Thorac Cardiovasc Surg 2006;132:332-9. 23. Fairman RM, Tuchek JM, Lee WA, Kasirajan K, White R, Mehta M, et al. Pivotal results for the Medtronic Valiant Thoracic Stent Graft System in the VALOR II trial. J Vasc Surg 2012;56:1222-31.e1. 24. Wong CS, Healy D, Canning C, Coffey JC, Boyle JR, Walsh SR. A systematic review of spinal cord injury and cerebrospinal fluid drainage after thoracic aortic endografting. J Vasc Surg 2012;56:1438-47. 25. Christiansson L, Ulus AT, Hellberg A, Bergqvist D, Wiklund L, Karacagil S. Aspects of the spinal cord circulation as assessed by intrathecal oxygen tension monitoring during various arterial interruptions in the pig. J Thorac Cardiovasc Surg 2001;121:762-72. 26. Strauch JT, Spielvogel D, Lauten A, Zhang N, Shiang H, Weisz D, et al. Importance of extrasegmental vessels for spinal cord blood supply in a chronic porcine model. Eur J Cardiothorac Surg 2003;24:817-24. 27. Biglioli P, Roberto M, Cannata A, Parolari A, Fumero A, Grillo F, et al. Upper and lower spinal cord blood supply: the continuity of the anterior spinal artery and the relevance of the lumbar arteries. J Thorac Cardiovasc Surg 2004;127:1188-92. 28. Laschinger JC, Cunningham JN Jr, Cooper MM, Krieger K, Nathan IM, Spencer FC. Prevention of ischemic spinal cord injury following aortic cross-clamping: use of corticosteroids. Ann Thorac Surg 1984;38:500-7. 29. Kunihara T, Matsuzaki K, Shiiya N, Saijo Y, Yasuda K. Naloxone lowers cerebrospinal fluid levels of excitatory amino acids after thoracoabdominal aortic surgery. J Vasc Surg 2004;40:681-90. 30. Reilly LM, Rapp JH, Grenon SM, Hiramoto JS, Sobel J, Chuter TA. Efficacy and durability of endovascular thoracoabdominal aortic aneurysm repair using the caudally directed cuff technique. J Vasc Surg 2012;56:53-63; discussion: 63-4. 31. Guillou M, Bianchini A, Sobocinski J, Maurel B, D’Elia P, Tyrrell M, et al. Endovascular treatment of thoracoabdominal aortic aneurysms. J Vasc Surg 2012;56:65-73. Submitted Sep 26, 2012; accepted Dec 6, 2012.
Low incidence of paraplegia after thoracic endovascular aneurysm repair with proactive spinal cord protective protocols Joseph L. Bobadilla, MD,a Martha Wynn, MD,b Girma Tefera, MD,c and C. W. Acher, MD,c Lexington, Ky; and Madison, Wisc Objective: Paraparesis and paraplegia after thoracic endovascular aneurysm repair (TEVAR) is a greatly feared complication. Multiple case series report this risk up to 13% with no, or inconsistent, application of interventions to enhance and protect spinal cord perfusion. In this study, we report our single-institution experience of TEVAR, using the same proactive spinal cord ischemia protection protocol we use for open repair. Methods: Endovascular thoracic aortic interventions were performed for both on-label (aneurysm) and off-label (trauma, other) indications. Aortic area covered was recorded as a fraction from the subclavian to celiac origins and reported as a percentage. If debranching was required, measurements were taken from the most distal arch vessel left intact. Intraoperative imaging and postoperative computed tomographic angiogram were used in calculating aortic percent coverage. Outcomes were recorded in a clinical database and analyzed retrospectively. The spinal cord ischemia protection included routine spinal drainage (spinal fluid pressure <10 mm Hg), endorphin receptor blockade (naloxone infusion), moderate intraoperative hypothermia (<35 C), hypotension avoidance (mean arterial pressure >90 mm Hg), and optimizing cardiac function. Results: From 2005 to 2012, 94 consecutive TEVARs were studied. Indications were thoracic aneurysm (n [ 48), plaque rupture with or without dissection (n [ 23), trauma (n [ 15), and other (n [ 8). Forty-nine percent were acute, average age was 68.5 years, 60% (n [ 56) were male, and the mean follow-up was 12 months. Mean length of aortic coverage was 161 mm, correlating to 59.4% aortic coverage. One patient had delayed paralysis (1.1%; observed/expected ratio, 0.12) and recovered enough to ambulate easily without assistance. Other complications included wound (7.5%), stroke (4.3%), myocardial infarct (4.3%), and renal failure (1.1%). Conclusions: Proactive spinal cord protective protocols appear to reduce the incidence of spinal ischemia after TEVAR compared with historical series. This study would suggest that active, as opposed to reactive, approaches to spinal ischemia portend a better long-term outcome. Multimodal protection is essential, especially if long segment coverage is planned. (J Vasc Surg 2013;57:1537-42.)
Over the last 3 decades, great progress has occurred in reducing the incidence of spinal cord ischemia and paralysis after open thoracic aortic aneurysm repair.1,2 From the initial observation of the artery of Adamkiewicz nearly 150 years ago, to its implication in neurologic complications after aortic surgery over the past 50 years,3 to a more complex understanding of the collateral network concept,4 the rate of paraplegia after thoracic aortic surgery has declined slowly over time.1 It has been shown in open From the Department of Surgery, Vascular and Endovascular Surgery, University of Kentucky, Lexingtona; and the Department of Anesthesiologyb and Department of Surgery, Division of Vascular Surgery,c School of Medicine and Public Health, University of Wisconsin, Madison. Author conflict of interest: none. Presented in Poster Form at the Thirty-sixth Annual Meeting of the Midwestern Vascular Surgical Society, Milwaukee, Wisc, September 6-8, 2012. Reprint requests: Joseph L. Bobadilla, MD, Department of Surgery, University of Kentucky, 800 Rose St, Room C219 Lexington, KY 40536-0293 (e-mail: [email protected]). The editors and reviewers of this article have no relevant financial relationships to disclose per the JVS policy that requires reviewers to decline review of any manuscript for which they may have a conflict of interest. 0741-5214/$36.00 Published by Elsevier Inc. on behalf of the Society for Vascular Surgery. http://dx.doi.org/10.1016/j.jvs.2012.12.032
aneurysm repair that multimodal protocols to protect and augment spinal perfusion are essential in reducing the incidence of this disabling complication.1,2,5-11 Furthermore, consistent and uniform application of these protocols is essential, as demonstrated by Hollier et al, where spinal ischemia was reduced from 6% to 0% over an 11-year period with the implementation of a proactive protocol.12 As the application of endovascular aneurysm repair has progressed to include thoracic pathologies, these theories again need to be revisited. Over the last decade, it has become increasingly apparent that thoracic endovascular aneurysm repair (TEVAR) carries the same risk of paraparesis/paraplegia as open thoracic aortic repair.13-17 A recent review by Rizvi and Sullivan estimated the overall risk of paraplegia/paraparesis after TEVAR to be 3.9%. This was based on a meta-analysis of 5349 patients in over 50 published reports. More importantly, the rate of paraplegia ranged from 0% to 13.3% among the reported case series, each with variable spinal cord protection protocols and inconsistent implementation.16 It is clear that with inconsistent application of interventions to enhance and protect spinal cord perfusion, paraplegia rates can be unnecessarily and unacceptably high.12,16 We have previously shown that aggressive spinal 1537
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fluid drainage is effective in reducing spinal cord ischemia, with an acceptable risk profile.18 The goals of any effective spinal protection protocol include increasing the spinal perfusion pressure, buffering the ischemia-reperfusion injury, and reducing the spinal cord metabolic demand. Specific interventions, either chemical or mechanical, addressing each of these fundamental points synergistically increase perfusion while reducing the ischemia/reperfusion response, neuronal metabolic activity, and excitotoxicity. In this study, we report our single-institution experience of TEVAR, using the same proactive spinal cord ischemia protection protocol we use for open aneurysm repair. This protocol consists of uniform spinal fluid drainage, permissive mild hypothermia, increasing mean arterial blood pressure, and multimodal pharmico-prophylaxis. METHODS During a 7-year contiguous period from January 1, 2005 to January 31, 2012, all TEVARs were prospectively enrolled into our institutional clinical database. Demographic data, clinical comorbidities, and outcomes data were recorded. In addition, postoperative complications including endoleak, wound-related complications, stroke, myocardial infarction, renal failure, paraplegia/paraparesis, and death were also monitored and recorded. All patients receiving a Food and Drug Administrationapproved thoracic endovascular device were included in analysis, regardless of on- or off-label indication for implantation. Both elective and emergent presentations were included in this cohort, as well as patients requiring either abdominal or cervical arch debranching procedures to ensure proper landing zone. Trauma patients with short segment coverage using extension cuff segments were excluded from this study. In standard TEVAR implantations, those patients not requiring a debranching procedure, aortic length covered was recorded, in centimeters, as a fraction from the left subclavian to celiac origins. Measurements were taken utilizing the intraoperative imaging and first postoperative computed tomographic angiogram scan. If either abdominal or arch debranching procedures were required to assure adequate landing zone, measurements were taken from the most distal arch vessel left intact to the most proximal abdominal branch vessel left intact. Because of the confounding issue of differing absolute aortic lengths among patients, the length of aortic coverage was normalized by calculating a percent aortic coverage. These calculations were completed retrospectively. Total aortic graft coverage length was divided by the total aortic length, allowing for better comparison of normalized percent aorta covered among patients with variable absolute lengths covered. The spinal cord ischemia protection protocol included routine spinal drainage in all patients. Spinal drains were placed in all patients, regardless of elective or emergent presentation, so long as hemodynamic stability allowed. In the setting of unstable rupture, operative intervention without spinal drainage can be undertaken, but we strive
to obtain spinal drainage in all patients. All patients in this cohort received spinal drains, which were placed in the operating room by our dedicated cardiovascular anesthesiology group. Goals of drainage were to a spinal fluid pressure 8 mm Hg intraoperatively and 10 mm Hg postoperatively. This was accomplished by draining in 5 to 15 mL aliquots utilizing a buretrol system until the target pressure was achieved. All drainage was accomplished by gravity alone. There was no volume limit threshold at which spinal fluid drainage was ceased, although average intraoperative volumes ranged from 100 to 130 mL. If bloody fluid drainage was noted, the spinal drain was clamped, and a stat noncontrast head computed tomography was obtained to evaluate for extra-axial hemorrhage. In uncomplicated cases, spinal fluid drainage was stopped and the spinal drain clamped once brisk lower extremity leg lifting was reproducibly present on physical examination. Spinal drains were routinely removed 24 to 48 hours after surgery. All patients received methylprednisolone 30 mg/kg after anesthetic induction, up to a maximum dose of 2 g. Patients also received mannitol, 12.5 g shortly after anesthesia induction. Mannitol has been shown to reduce cerebrospinal fluid pressures experimentally and clinically. Experimentally, mannitol has also been shown to function as a free-radical scavenger and serve as an osmotic diuretic with renal protective properties.19 Moderate intraoperative hypothermia was allowed through radiative loss and the administration of cold intravenous fluids, to a goal temperature of less than 35 C, but more than 32 C. Postoperatively, active rewarming (thermal warming blankets) was strictly avoided, only ambient rewarming was allowed. Active rewarming blankets were avoided because of the potential induction of peripheral vasodilation. This can result in shunting of blood away from central structures, including the spinal cord. Reduced blood flow coupled with increased temperature and metabolic demands are major contributors to spinal ischemia risk. During both the intraoperative and postoperative time frames, mean arterial blood pressures were kept >85 mm Hg. In addition, patients were maintained on a continuous naloxone infusion starting before anesthesia induction and lasting for 24 hours postoperatively. Naloxone infusion was prepared with 2.5 mg in 250 mL diluent (10 mcg/mL) and infused at 1 mcg/kg/h. RESULTS From 2005 to 2012, 94 consecutive TEVAR implantations were studied. All procedures were performed at a single institution. Indications for repair included degenerative thoracic aneurysm (n ¼ 48), plaque rupture/intramural hematoma (n ¼ 23), trauma (n ¼ 15), and other (n ¼ 8). The other group included acute type B dissection (n ¼ 3), pseudoaneurysm (n ¼ 4), and one patient with presumed aortoesophageal bleeding. There were no patients with known connective tissue disorders included in this study cohort. The mean aortic diameter at the time of intervention for those patients with a degenerative aneurysm was 6.5 cm (minimum, 5.6 cm; maximum,
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9.0 cm). Plaque rupture was defined as new evidence of ulcerated plaque or intramural hematoma with symptoms, including back or chest pain. All trauma patients with evidence of intimal disruption, intramural hematoma, or extravasation were considered for TEVAR. Indication for TEVAR in acute type B dissection included renovisceral or limb malperfusion. The mean follow-up time period was just over 12 months. Debranching procedures were required in 17 cases (18.1%); of these, 15 were arch debranchings and two abdominal debranchings. Any patient requiring extension of the proximal landing zone underwent debranching at the time of TEVAR, or in a staged procedure prior to TEVAR. All patients underwent prophylactic debranching preceding TEVAR. There were 14 subclavian transposition/bypass procedures completed. One patient underwent both left subclavian and left common carotid revascularization in preparation for TEVAR. Both abdominal debranching procedures consisted of four-vessel revascularization: celiac/hepatic, superior mesenteric artery, and both renal arteries. Comorbidities of the group are listed in Table I. The mean length of aortic coverage was 161 mm, and the average normalized aortic percent coverage was 59.4% of total aortic length. There were 10 endoleaks identified during the course of the study. Seven of these were either type Ia or Ib leaks; these were all treated with proximal or distal extension. There was one type III leak treated with a bridging device, and two type II leaks with no sac expansion that ultimately thrombosed on their own. There were no cases of paraplegia or paralysis related to the repeat interventions. There was one patient who developed a cold leg after percutaneous closure device failure resulted in common femoral artery occlusion. This was removed operatively with no long-term adverse sequaelae. In addition, seven (7.4%) patients developed wound breakdown or superficial wound infections. There were four patients each who suffered perioperative myocardial infarction or cerebrovascular accident (Table II). There was one delayed paralysis (1.1%; observed/ expected ratio, 0.12). This patient had undergone elective TEVAR covering the proximal 63% of the native aorta along with arch debranching with a subclavian transposition for aneurysmal disease, patient number 37 (Fig). The paraplegia was associated with a period of postoperative hypotension. It responded to aggressive blood pressure augmentation and fluid resuscitation. The patient was able to recover and ambulate easily without assistive devices at the time of discharge. During the course of the study, there were no other patients that presented with delayed paraplegia. There were seven deaths during the course of this study. The mean time to death after TEVAR in these patients was 1.1 years (range, 0.72-1.86 years). Six of these were after hospital discharge and >30 days from the index case. There was one intraoperative death in this cohort. This was an 87-year-old female who presented with an acute plaque rupture and extensive intramural hematoma.
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Table I. Patient characteristics Category
Value (%)
Age, years Sex Male Female Presentation Elective Emergent Indication Thoracic aneurysm Plaque rupture/hematoma Trauma Other Procedure Standard TEVAR TEVAR þ arch debranching TEVAR þ abdominal debranching Comorbidities None Coronary artery disease Chronic obstructive pulmonary disease Diabetes Hypertension ASA score ASA 1 ASA 2 ASA 3 ASA 4 ASA 5 ASA 6
54 6 15 56 (60) 38 (40) 48 (51) 46 (49) 48 23 15 8
(51) (24) (16) (9)
77 (82) 15 (16) 2 (2) 14 30 20 2 75
(15) (32) (21) (2) (80)
0 4 36 46 8 0
(0) (4) (38) (49) (8) (0)
ASA, American Society of Anesthesiologists; TEVAR, thoracic endovascular aneurysm repair. Summary data of patient demographics, acuity of presentation, indication for operation, and comorbid conditions in all 94 TEVAR patients.
Table II. Patient data and outcomes Category
Value (%)
Mean aortic length coverage, mm Mean aortic coverage, % Complications Endoleak Wound breakdown/infection Stroke Myocardial infarct Acute renal failure Paraplegia Death
161 6 73 59.4 6 19 10 7 4 4 1 1 7
(10.6) (7.4) (4.3) (4.3) (1.1) (1.1) (7.4)
TEVAR, Thoracic endovascular aneurysm repair. Summary of mean aortic distance (mm) and percent aortic coverage along with postoperative outcomes data in all 94 TEVAR patients.
Upon device deployment, the patient became precipitously hypotensive. Repeat angiogram showed proximal conversion to free rupture into the left chest. A second device was brought on the field to deploy more proximally, but the patient ultimately expired in the operating room. There was one complication related to spinal drain placement in this patient group. This patient developed an epidural hematoma with cord compression after he was started on low-molecular-weight heparin. He had
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Fig. Percent aortic coverage. Each of the 94 patients in this study is represented by a single bar in this figure and numbered 1 to 94 accordingly. Patients are presented sorted by coverage extent and not chronological order for ease of interpretation. The open white bars represent proximal and/or distal uncovered aortic segments, measured as a percent of total aortic length. The blue shaded bar represents the percent of aorta covered with the thoracic endovascular aneurysm repair (TEVAR) devices. Patients requiring debranching procedures are noted by the blue (arch debranching) and purple (abdominal debranching) highlighted circles overlying the patient numbers. The solitary paraplegia patient, number 37, is also denoted with a red highlighted circle.
a history of aortic valve. He returned to our emergency room on postoperative day 6 with low back pain and bilateral lower extremity pain and weakness. Imaging revealed the epidural hematoma, and urgent decompressive laminectomy was completed. He regained function and recovered uneventfully. DISCUSSION In this study, we have examined the outcomes related to paraplegia and paraparesis after TEVAR with an aggressive and proactive spinal cord protection protocol. We observed an overall paraplegia event rate of 1.1%, much lower than other reported case series. In addition, this rate is lower than those results of the major multicenter international registry papers (European Collaborators on Stent Graft Techniques for Thoracic Aortic Aneurysm and Dissection Repair [EUROSTAR], 4.0%; GORE TAG
thoracic endoprosthesis registry [GORE-TAG], 3%; Talent Thoracic Retrospective Registry [TTR], 1.7%; Valiant Thoracic Stent Graft System Clinical Study [VALOR II], 2.5%).20-23 A recent meta-analysis review of published studies related to spinal protection showed an overall rate of paraplegia/paraparesis of 3.88%. Among those groups that employed routine spinal fluid drainage (SFD), this rate was 3.2%. Among those that never used SFD, the rate was 3.47%, and lastly, among those who selectively practiced SFD, the rate was 5.6%.24 Although our study is limited by the relatively low number of patients and heterogeneous pathologies, we believe it illustrates an essential concept about spinal cord perfusion and protection. Spinal cord perfusion during and after thoracic aortic surgery, including TEVAR, is maintained by a complex interplay between perfusion pressure, collateral networks, and the ischemia-reperfusion response. The ultimate goal
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of spinal cord protection must be the prevention of paraplegia/paraparesis using proactive measures and not rescue after it has already ensued. The consequences of failure to rescue are too great given the relatively simple and lowrisk prophylactic measures that can be implemented. In humans, the artery of Adamkiewicz has variable origin and is presumed to give rise to the greater radicular artery, a major feeder to the anterior spinal artery and perfusion source for the ventral motor columns.3 In addition, spinal cord blood flow is a plexus circulation with collateral feed from other intercostal radicular arteries, subclavian, vertebral, hypogastric, and other collateral contributors.25-27 When these collateral networks become compromised, or sacrificed, because of aortic surgery, spinal perfusion can suffer, and paraplegia may result.4 Certain patients are at increased risk for disruption of the plexus network. Those who have had prior aortic surgery, those with hypogastric or left subclavian stenosis/occlusion, and those with occluded lumbar arteries are at increased risk because of reduced inputs. In addition, those patients who require a long segment of thoracic coverage are at higher risk because of increased blood flow disruption. The more open intercostal arteries covered during TEVAR, the higher the risk of resulting paraplegia/paraparesis. It is because of the complex interplay of all these variables that spinal protection must be undertaken, especially in high-risk patients. Unfortunately, no single variable, or group of characteristics, can completely predict which patients will develop paraplegia/paraparesis post-TEVAR. Because of this, and the low morbidity associated with the interventions we utilize, we support the routine use of this proactive multimodal spinal protection in all patients undergoing formal TEVAR. The goals of spinal cord perfusion protection during thoracic aortic intervention are threefold: prolong spinal cord ischemic tolerance, reduce the ischemia reperfusion response, and improve spinal cord oxygen delivery. Improved ischemic tolerance can be accomplished with mild intraoperative hypothermia. We typically cool to 34 C. This helps to reduce spinal cord metabolic activity and spinal cord oxygen requirements. Ischemia-reperfusion injury can be attenuated with the routine use of induction steroid bolus to stabilize cellular membranes and minimize local inflammatory response pathways.28 In addition, naloxone infuse has been shown to reduce the release of excitatory neurotransmitters from ischemic neurons.29 Finally, mannitol acts as a free-radical scavenger, helping to blunt the reperfusion injury response.19 The third factor, spinal cord oxygen delivery, is the summation of hemodynamic and oxygen content factors. Blood flow is perhaps best visualized by the equation spinal cord perfusion pressure equals mean arterial blood pressure minus spinal fluid pressure. With this relationship, it is clear that augmentation of cardiac function and reduction in spinal fluid pressure are key to preserving spinal perfusion. We routinely employ spinal fluid drainage to augment microvascular perfusion. We choose an intraoperative drainage threshold of 8 mm Hg and
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a postoperative threshold of 10 mm Hg. This is in part because of our observations with open thoracic aortic surgery. We have noted a higher incidence of paraplegia/paraparesis in those patients with spinal fluid pressures over 10 mm Hg. Two recent studies have confirmed the observation that more aggressive spinal fluid drainage improves paraplegia/paraparesis rescue.30,31 The risks of spinal fluid drainage are low, and we believe are offset by the benefits derived from paraplegia prevention.18 We recommend holding prophylactic heparin dosing the morning of spinal drain removal and for the next 6 to 8 hours after drain removal. Obviously, adequate hemoglobin and oxygen are necessary to provide adequate tissue oxygen delivery, and avoidance of hypotension, hypoxemia, and anemia during and after intervention is essential. Oxygen delivery is directly dependent upon oxygen content, and we routinely strive for hemoglobin concentrations $10 g/dL. The use of active warming blankets can cause peripheral vasodilation, resulting in diversion of blood flow from central structures, including the spinal cord. For this reason, we advocate passive rewarming, which has the added benefit of maintaining reduced neuronal metabolic demands during this critical perioperative phase. When patients present with delayed paraplegia, we advocate the routine use of spinal fluid drainage and pharmacologic elevation of blood pressure to a mean pressure of 85 mm Hg or greater. Although endovascular thoracic aortic repair clearly provides an overall reduction in much of the morbidity associated with open thoracic aortic repair, paraplegia does not appear to be significantly reduced. TEVAR presents a unique insult to the spinal plexus network, with abrupt, oftentimes, long-segment input disruption and the added risk of embolization from lateral displacement of lining thrombus. In addition, this often occurs at relatively normothermic body temperatures, further amplifying the resulting ischemic injury. Because of this, we advocate a consistent approach to the prevention of paralysis/paraparesis during TEVAR based on the pathophysiology of spinal cord ischemia. We utilize the same multimodal protocol that is used during our open thoracic aneurysm repairs. Careful attention to cardiac function, perfusion pressure, spinal fluid pressure, along with chemoprophylaxis has reduced the incidence of spinal ischemia in our hands to roughly 1%, regardless of elective or emergent presentation. CONCLUSIONS Proactive spinal cord protective protocols appear to reduce the incidence of spinal ischemia after TEVAR when compared to historical series. This study would suggest that active, as opposed to reactive, approaches to spinal ischemia portend a better long-term outcome. The ultimate goal of spinal cord protection must be the prevention of paraplegia/paraparesis using proactive measures and not rescue after it has already occurred. The consequences of failure to rescue are too great given the relatively simple and low-risk prophylactic measures that can
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be implemented preemptively. Multimodal protection is essential, especially if long-segment coverage is planned. These strategies should include specific interventions directed toward improving spinal cord ischemic tolerance, reducing the ischemia reperfusion response, and improving spinal cord oxygen delivery. AUTHOR CONTRIBUTIONS Conception and design: JB, MW, GT, CA Analysis and interpretation: JB, MW, GT, CA Data collection: JB Writing the article: JB Critical revision of the article: JB, MW, GT, CA Final approval of the article: JB, MW, GT, CA Statistical analysis: JB, CA Obtained funding: Not applicable Overall responsibility: JB REFERENCES 1. Acher CW, Wynn M. A modern theory of paraplegia in the treatment of aneurysms of the thoracoabdominal aorta: an analysis of technique specific observed/expected ratios for paralysis. J Vasc Surg 2009;49: 1117-24; discussion: 1124. 2. Acher C, Wynn M. Outcomes in open repair of the thoracic and thoracoabdominal aorta. J Vasc Surg 2010;52:3S-9S. 3. Adams HD, Van Geertruyden HH. Neurologic complications of aortic surgery. Ann Surg 1956;144:574-610. 4. Griepp RB, Griepp EB. Spinal cord perfusion and protection during descending thoracic and thoracoabdominal aortic surgery: the collateral network concept. Ann Thorac Surg 2007;83:S865-9; discussion: S890-2. 5. Mell MW, Wynn MM, Reeder SB, Tefera G, Hoch JR, Acher CW. A new intercostal artery management strategy for thoracoabdominal aortic aneurysm repair. J Surg Res 2009;154:99-104. 6. Acher CW, Wynn MM, Mell MW, Tefera G, Hoch JR. A quantitative assessment of the impact of intercostal artery reimplantation on paralysis risk in thoracoabdominal aortic aneurysm repair. Ann Surg 2008;248:529-40. 7. Tefera G, Acher CW, Wynn MM. Clamp and sew techniques in thoracoabdominal aortic surgery using naloxone and CSF drainage. Semin Vasc Surg 2000;13:325-30. 8. Acher CW, Wynn MM, Hoch JR, Kranner PW. Cardiac function is a risk factor for paralysis in thoracoabdominal aortic replacement. J Vasc Surg 1998;27:821-8; discussion: 829-30. 9. Acher CW, Wynn MM. Multifactoral nature of spinal cord circulation. Seminars in thoracic and cardiovascular surgery 1998;10:7-10. 10. Acher CW, Wynn MM, Hoch JR, Popic P, Archibald J, Turnipseed WD. Combined use of cerebral spinal fluid drainage and naloxone reduces the risk of paraplegia in thoracoabdominal aneurysm repair. J Vasc Surg 1994;19:236-46; discussion: 247-8. 11. Acher CW, Wynn MM, Archibald J. Naloxone and spinal fluid drainage as adjuncts in the surgical treatment of thoracoabdominal and thoracic aneurysms. Surgery 1990;108:755-61; discussion: 761-2. 12. Hollier LH, Money SR, Naslund TC, Proctor CD Sr, Buhrman WC, Marino RJ, et al. Risk of spinal cord dysfunction in patients undergoing thoracoabdominal aortic replacement. Am J Surg 1992;164:210-3; discussion: 213-4. 13. Maeda T, Yoshitani K, Sato S, Matsuda H, Inatomi Y, Tomita Y, et al. Spinal cord ischemia after endovascular aortic repair versus open surgical repair for descending thoracic and thoracoabdominal aortic aneurism. J Anesth 2012:1-7.
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