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Original Articles: Adult Cardiac

Extent of Aortic Coverage and Incidence of Spinal Cord Ischemia After Thoracic Endovascular Aneurysm Repair

^a Division of Vascular Surgery and Endovascular Therapy, University of Florida, Gainesville, Florida
^b Division of Thoracic and Cardiovascular Surgery, Department of Surgery, University of Florida, Gainesville, Florida
^c Division of Biostatistics, Department of Epidemiology and Biostatistics, University of Florida, Gainesville, Florida

Accepted for publication September 4, 2008.

^_* Address correspondence to Dr Lee, Division of Vascular Surgery and Endovascular Therapy, 1600 SW Archer Rd, Ste NG-45, PO Box 100286, Gainesville, FL 32610-0286 (Email: anthony.lee{at}surgery.ufl.edu).

Presented at the Forty-fourth Annual Meeting of The Society of Thoracic Surgeons, Fort Lauderdale, FL, Jan 28–30, 2008.

	Abstract

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Background: Risk factors for spinal cord ischemia (SCI) after thoracic endovascular aneurysm repair (TEVAR) remain unclear. Aortic coverage was examined as a risk factor for SCI using quantitative three-dimensional computed tomography angiography (CTA) analysis.

Methods: The medical records, radiographic imaging studies, and a prospectively maintained database of all TEVAR procedures performed during a 7-year period were retrospectively reviewed. Preoperative anatomic dimensions and postoperative graft path lengths were measured from CTAs using curved planar and orthogonal multiplanar reformations along centerline paths. SCI was defined as transient or permanent lower extremity neurologic deficit without associated intracerebral hemispheric events.

Results: Of 326 TEVAR cases, 241 patients (74%) had satisfactory imaging. Thirty-three (10%) had SCI. These patients were older (72.7 ± 10.6 vs 64.7 ± 15.8 years, p = 0.005) and had longer intraoperative procedure times (137 ± 65 vs 113 ± 68 minutes, p = 0.05). Despite similar total lengths of native thoracic aorta (295.0 ± 36.3 vs 283.1 ± 39.8 mm, p = 0.17), patients with permanent SCI had a greater absolute (260.5 ± 40.9 vs 195.8 ± 81.6 mm, p = 0.002) and proportionate (88.8% ± 12.1% vs 67.6% ± 24.0%, p = 0.001) length of aortic coverage. The average length of uncovered aorta proximal to the celiac artery in patients with SCI was 17.3 ± 21.8 mm vs 63.1 ± 62.9 mm in patients without SCI (p = 0.0006). Neither the patency of the hypogastric arteries nor left subclavian artery was associated with SCI.

Conclusions: The extent and distal location (relative to the celiac artery) of aortic coverage were associated with an increased risk of SCI. Prophylactic measures for spinal cord protection should be considered in patients whose thoracic aortas require extensive coverage.

	Introduction

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Spinal cord ischemia (SCI) is a devastating complication after surgical or endovascular repair (TEVAR) of the thoracic aorta. The results from the W. L. Gore TAG (Flagstaff, AZ) pivotal trial reported a 30-day incidence of SCI of 3% [1], which was significantly lower than that reported with open surgical repair. Risk factors for SCI after TEVAR are multifactorial and have been previously reported to include length of aortic coverage [2], prior abdominal aortic aneurysm (AAA) repair [3], hypotension [4], iliac artery injury [5], renal failure [6], and left subclavian artery coverage [6].

Although the putative mechanism of loss of direct intercostal perfusion in SCI appears intuitive, occurrence of symptoms are inconsistent and seemingly unpredictable. In this study we examined the role of thoracic aortic coverage by the endograft in the development of SCI using quantitative analysis of preoperative and postoperative computed tomography angiography (CTA) data sets.

	Material and Methods

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The medical records, radiographic imaging studies, and a prospectively maintained database of all thoracic endovascular procedures performed at a single tertiary-care medical center between September 2000 and May 2008 were retrospectively reviewed. CTA of the chest, abdomen, and pelvis was performed using a timed-bolus, intravenous contrast–enhanced technique acquired at 2-mm collimation. The data set was reconstructed and postprocessed using the Aquarius Workstation (TeraRecon, San Mateo, CA). Anatomic dimensions and endograft path lengths were measured from three-dimensional (3D) reconstructions using curved planar and orthogonal multiplanar reformation along centerline paths. The first postoperative CTA, which was typically performed either before discharge or at 1-month, was compared with the preoperative CTA.

SCI was defined as any new lower extremity motor or sensory deficit, or both, in the absence of any documented intracerebral hemispheric events. A patient who was fully ambulatory preoperatively must have been able to bear his or her own weight without assistance to be considered neurologically intact. SCI was considered transient (vs permanent) when a clear deficit was documented and then fully resolved at the time of discharge. When a patient's symptoms had improved but his or her functional status was not completely restored to preoperative levels, the complication was considered permanent.

Spinal drainage was not performed prophylactically in most patients. Patients were admitted postoperatively to the cardiac intensive care unit, where neurologic exams were performed hourly. Upon detection of symptoms, the blood pressure was elevated to a systolic pressure of more than 160 mm Hg (mean arterial pressure of > 100 mm Hg) with vasopressors or fluids, or both, and if it had not been performed preoperatively, a spinal drainage catheter was promptly (< 2 hours of symptoms) inserted by a cardiac anesthesiologist. The catheter was placed 10 cm above the level of the heart and adjusted higher or lower depending on therapeutic effect and amount of spinal fluid drainage. Drainage was limited to less than 15 mL/h or 350 mL/24 h to avoid potential complications of subdural hematoma or cerebral herniation. The catheter was left to drain for 72 hours. If therapeutic effect was achieved, the catheter was clamped for another 24 hours in case symptoms returned, and then it was removed.

Continuous data were analyzed using a two-tailed t test and categoric variables using the Fisher exact test, with p < 0.05 considered statistically significant. Univariate and multivariate logistic regression models were constructed using a set of 20 potential predictors: age, sex, American Society of Anesthesiologists (ASA) classification, urgency of the procedure, total duration of procedure, fluoroscopy time, contrast volume, preoperative spinal drainage, endograft type, anesthetic technique, blood loss, use of an iliac conduit, history of AAA repair, aortic pathology, total thoracic aortic length (from left common carotid artery to celiac artery), length of total aortic coverage, length of proximal uncovered aorta, length of distal uncovered aorta, left subclavian artery (L SCA) perfusion, and hypogastric artery patency. Odds ratio (OR) estimates were reported with 95% confidence intervals (CIs).

This study was approved by the Institutional Review Board with waiver of informed consent.

	Results

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Between September 2000 and May 2008, 326 TEVARs were performed. The mean age of the patients was 65.5 ± 15.5 years, and 222 (68%) were men. Comorbidities included hypertension (69%), coronary artery disease (49%), tobacco use (42%), chronic obstructive pulmonary disease (20%), renal insufficiency (16%), cerebrovascular occlusive disease (13%), diabetes mellitus (12%), and peripheral vascular occlusive disease (9%). Postoperative complications occurred in 121 patients (37.1%) comprising 57 neurologic (17%), 26 pulmonary (8%), 21 renal (6%), 20 hemorrhagic (6%), 17 ischemic (5%), 13 cardiac (4%), 8 wound (2%), and 7 gastrointestinal (2%) complications. Overall median length of stay was 5 days (range, 1 to 79 days) and 30-day or in-hospital mortality was 7.4% (24 of 326). Kaplan-Meier estimates of late mortality were 81%, 74%, and 66% at 6, 12, and 24 months, with a median survival of 42.3 months.

SCI occurred in 33 patients, (10%) of SCI, and 14 (4%) were permanent. The distribution of aortic pathologies treated and the incidence of SCI in each category are compiled in Table 1. Univariate analyses of preoperative and intraoperative risk factors in the development of any SCI and the subset that had permanent SCI are summarized in Table 2. Any (temporary or permanent) SCI was associated with age (72.7 ± 10.6 vs 64.7 ± 15.8 years, p = 0.005), procedure time (137 ± 65 vs 113 ± 68 minutes, p = 0.05), fluoroscopy time exceeding 35 minutes (27% vs 13%, p = 0.04), and general anesthesia (82% vs 64%, p = 0.05). Variables not associated with SCI included gender, ASA classification, urgency of procedure, the device implanted, blood loss, the use of an iliac conduit, prior AAA repair, and the pathology being treated.

Quantitative 3D-CTA Analysis
Satisfactory preoperative and postoperative CT angiograms were available in 241 patients (74%), 23 of whom had SCI (9%). The reasons for exclusion of the remaining 85 patients are listed in Table 3. Select baseline characteristics of those with and without adequate imaging were compared (Table 4) to ascertain that the former subset was representative of the overall cohort. The only significant difference was a higher proportion of traumatic aortic transections among those with adequate imaging (8% vs 1%, p = 0.02). More importantly, the incidences of any (10% vs 12%, p = 0.54) and permanent (4% vs 6%, p = 0.37) SCI were similar between those who did and did not have adequate imaging.

SCI was strongly associated with the distal extent of thoracic aortic coverage. The mean length of uncovered aorta proximal to the celiac artery was 17.3 ± 21.8 mm in patients with SCI compared with 63.1 ± 62.9 mm in those without SCI (p = 0.0001). When expressed as a fraction of the total aortic length, SCI patients had relatively less uncovered aorta distally (5.7% ± 7.0% vs 23.8% ± 24.6%, p = 0.0001; Fig 1A and B). This difference was also seen between those who had transient and permanent SCI (22.4 ± 25.6 mm vs 8.4 ± 8.3 mm, p = 0.06). On the other hand, the extent of proximal coverage as measured by the distance from the left common carotid artery to the proximal covered edge of the endograft did not differ between SCI and no-SCI patients (absolute 23.7 ± 24.4 mm vs 25.8 ± 38.4 mm, p = 0.80, fractional 7.9 % ± 8.2% vs 9.1% ± 13.7%, p = 0.68).

View larger version (72K): [in this window] [in a new window]   Fig 1. (A) Fractional coverage of the aorta in patients with spinal cord ischemia (SCI). (B) Fractional coverage of the aorta in patients without any SCI. The lengths of coverage have been normalized from the distal margin of the left common carotid artery to the proximal margin of the celiac artery.

	Comment

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Our current study examined the risk of SCI as a function of thoracic aortic coverage. We found that the total length of aortic coverage was greater in patients with SCI, with a mean difference of approximately 6.5 cm or 20% of the thoracic aorta. Furthermore, not only the absolute length but also the distal extent of coverage was strongly associated with SCI. Mechanistically, this secondary observation would be anatomically consistent given the distal origin of the Artery of Adamkiewicz (arteria magna), which arises from T11 to L3 levels.

The exact mechanism of SCI after thoracic aortic repair remains unclear and is clearly multifactorial. Spinal cord perfusion is a net function of highly variable and differential contributions from the intercostals [9] and their principle collateral vessels, namely the lumbar, vertebral, and hypogastric arteries [10], which can develop compensatory changes in chronic aortic diseases or after surgical aortic replacement. It stands to reason that any systemic conditions that result in hypoperfusion of these vessels, especially intercostal arteries, will also increase the chances of SCI [11].

Although an association between left subclavian artery coverage and SCI had been previously suggested [6], neither our study nor the one by Khoynezhad and colleagues [8] found such a correlation. Despite its apparent anatomic basis, the actual contribution to overall spinal cord perfusion by one or both proximal branches of the anterior spinal artery is difficult to determine, and we do not believe that this alone justifies prophylactic left subclavian artery revascularization. Currently, the main indications for preoperative subclavian artery bypass are a dominant left vertebral artery with a diminutive right vertebral artery or a patent left internal mammary artery graft to the left anterior descending coronary artery, or both. To this end, CTA imaging of the intracranial circulation is routinely performed as part of preoperative imaging. The incidence of symptomatic left arm claudication is extremely small, but in those rare instances revascularization may be performed electively in the postoperative period.

The association between prior AAA repair and SCI has also been inconsistent among published reports. The results in our study (2% vs 5%, p = 0.70) were similar to the results of the TAG pivotal trial (4.7% vs 2.1%, p = NS), which did not find any difference in the rates of SCI between those with and without prior AAA repair [1]. A history of abdominal aortic replacement is likely a surrogate marker for decreased spinal cord perfusion as it relates to the lumbar arteries. Similar to the anterior spinal artery, the contribution of this or any other single blood supply to the development of clinically significant SCI cannot be easily determined.

An important weakness of our study is the lack of adequate postoperative imaging data in 85 of the 326 patients (26%). In 34 of these excluded patients, they involved abdominal or aortic arch debranching procedures, and the extent of endograft coverage was outside the proximal or distal limits, or both, of our quantitative analysis. Of the remaining 51 patients, 35 (11%) had no postoperative imaging and 16 (5%) had inadequate imaging as a result of early death or lost follow-up because of transfer to another facility. It should be noted, however, that both the rates of any SCI and permanent SCI were similar between those with and without adequate imaging at 10% vs 12% (p = 0.54) and 4% vs 6% (p = 0.37), respectively.

In conclusion, using quantitative 3D analysis of CT angiograms, our study showed a significant association with the extent of aortic coverage and the development of SCI. The need for sufficient proximal and distal aortic fixation to achieve a successful short and long-term repair must be weighed against the increased risk of spinal cord ischemia, especially for distal thoracic pathologies. Therefore, in cases which require greater than 200 mm of thoracic aortic coverage or distal coverage within 20 mm of the celiac artery, prophylactic measures for spinal cord protection should be considered.

	Discussion

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DR WILLIAM L. HOLMAN (Birmingham, AL): That is an interesting study. It gives me some hope that this terrible complication can be minimized. The question I had is the duration of these measures, and whether they are prophylactic or not. Let's say you are placing an aortic stent with some periprocedural measure of neurologic function in place, and then things start to go bad. Presume that you drain CSF [cerebrospinal fluid], increase the blood pressure, and do other things with improvement of neurological function. How long must you maintain these special conditions and how will you know when it's safe to restore normal physiology without having spinal ischemia?

DR FEEZOR: Our typical course is to leave the spinal drain in place at a level of 10 cm of water for 24 hours. If the neurological events stabilize or improve, then we clamp the spinal drain for 24 additional hours, with ongoing neurologic monitoring, then remove the spinal drain if the patient remains asymptomatic.

As far as the blood pressure is concerned, generally we pharmacologically raise the systolic blood pressure to 160 to 180 mm Hg for 2 to 4 days.

DR ROBERT S. D. HIGGINS (Chicago, IL): Do you have any other insights about how you manage those dissection patients now with this information in hand?

DR FEEZOR: Endovascular treatment of aortic dissection is evolving. I think that when we anticipate greater lengths of coverage, we are more apt to put in spinal drains prophylactically. A little bit depends on the chronicity of dissection. Complicated acute dissections with malperfusion or rupture tend to have worse outcomes than chronic dissections.

	References

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