Vascular OnlineFirst, published on January 6, 2015 as doi:10.1177/1708538114565694
Case Report
An unusual cause of spinal cord ischemia after thoracic endovascular repair
Vascular 0(0) 1–3 ! The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1708538114565694 vas.sagepub.com
Issam Koleilat, Erin Moore, Tod Hanover and John Eidt
Abstract A 59-year-old left-handed man presented with chest pain and hypertension and was found to have an acute descending aortic dissection on imaging. After thoracic endovascular repair of the dissection, he developed left arm weakness and ischemia. Despite carotid-subclavian transposition, the patient was found to have persistent left triceps weakness as well as bilateral leg paresis. An urgent spinal drain was placed that improved his lower extremity deficit but did not greatly change his arm symptoms. Magnetic resonance imaging of the spine revealed previously undiagnosed severe multilevel spinal stenosis requiring operative decompression. To our knowledge, this is the first report of the contribution of cervical spinal stenosis to post-thoracic endovascular repair spinal ischemia.
Keywords Aortic dissection, TEVAR, spinal ischemia
Case A 59-year-old left-handed man presented with chest pain and hypertension. He reported cocaine use prior to presentation. He was employed as a landscaper. Imaging revealed a focal acute Type B aortic dissection confined to the proximal descending thoracic aorta. Despite aggressive blood pressure control, his pain persisted and he was offered thoracic endograft repair (TEVAR). He underwent placement of a 32 mm 120 mm Zenith TX2 endograft (Cook Medical) with partial coverage of the left subclavian artery using intravascular ultrasound (IVUS) and fluoroscopy (Figure 1) demonstrating complete occlusion of the false lumen. On postoperative day 1, he developed new onset left hand paresthesias and pain with loss of the left radial pulse. He also complained of bilateral leg and left arm weakness. He was taken to the operating room urgently for left carotid subclavian transposition. Postoperatively, he was found to have bilateral leg paresis. A spinal drain was placed and cerebrospinal fluid (CSF) was removed to reach a CSF pressure of 10 mmHg. His lower extremity paresis resolved completely over the next 12 h, and while his left arm symptoms improved overall, his weakness of the left triceps persisted. Magnetic resonance imaging (MRI) of the spine revealed severe multilevel disease with large disk protrusion and severe spinal stenosis at C3-7 with central
cord ischemia (Figure 2). Additionally, there was posterior central disk protrusion at L3-5. The patient underwent C3-7 laminoplasty with arch fixation. His residual left arm weakness slowly improved over several weeks of rehabilitation.
Discussion To our knowledge, this is the first report of cervical spinal stenosis contributing to post-TEVAR spinal ischemia associated with coverage of the left subclavian artery. We hypothesize that this patient had delayed thrombosis of his subclavian artery leading to ischemia in two vascular beds: the left arm as well as the cervical spinal cord. We believe that his left arm symptoms resulted from a combination of upper extremity arterial insufficiency as well as cervical cord ischemia. His cervical spondylosis with focal segmental spondylolithesis resulted in multilevel severe spinal stenosis that likely increased the vulnerability of the cervical cord to vascular injury. The patient’s spinal cord was Department of Vascular Surgery, Greenville Health Systems, Greenville, USA Corresponding author: Issam Koleilat, Greenville Health System, 701 Grove Road, Greenville, SC 29605, USA. Email: [email protected]
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Vascular 0(0)
Figure 1. Angiogram depicting focal aortic dissection (left). Excluded dissection with partial coverage of the left subclavian artery (right).
Figure 2. Cervical MRI demonstrating severe cervical spondylosis with focal segmental spondylolithesis resulting in severe spinal stenosis of C3-7. MRI, magnetic resonance imaging.
compromised due the ‘‘pincer effect’’: compression by a hypertrophied ligamentum flavum posteriorly and protruding calcified disc anteriorly. As a result of the cord’s compromised physiology, it was particularly sensitive to further insults, both ischemic and compressive. Thus, the spinal cord edema from ischemia may have
been asymptomatic, but there was significantly reduced space in the spinal canal due to the undiagnosed spinal stenosis. While impossible to prove, we suspect that the ischemic insult was indirectly magnified by the presence of spinal compression. This vulnerability to ischemic injury has not been quantified in the literature, but is widely accepted theoretically. To date there are no reports of spinal cord ischemia after TEVAR exacerbated by cervical spinal stenosis. Currently described risk factors include coverage length (especially greater than 200 millimeters), coverage of T8-T12 intercostal vessels, prior abdominal aortic aneurysm repair, postoperative hypotension and left subclavian artery coverage.1,2 More recent data indicate that coverage of at least two of the four vascular territories that supply the spinal cord (left subclavian, intercostal, lumbar and hypogastric arteries) are needed to produce symptomatic spinal ischemia.3 We therefore suggest that preexisting severe spinal cord compression may additionally predispose patients undergoing TEVAR to spinal cord ischemia. In summary, it is likely that cervical spinal stenosis increases the vulnerability of the spinal cord to ischemic injury. In the setting of significant cervical spinal stenosis, we recommend prophylactic revascularization of the left subclavian artery prior to planned coverage during TEVAR.
Patient consent The patient described herein had given consent to the use of deidentified patient data for use in research and education as per institutional policy.
Downloaded from vas.sagepub.com at University of Otago Library on October 11, 2015
Koleilat et al.
3
Conflict of interest None declared.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. Buth J, Harris PL, Hobo R, et al. Neurologic complications associated with endovascular repair of thoracic aortic pathology: Incidence and risk factors. A study from the
European Collaborators on Stent/Graft Techniques for Aortic Aneurysm Repair (EUROSTAR) registry. J Vasc Surg 2007; 46: 1103–10. (discussion 10–1). 2. Matsumura JS and Rizvi AZ. Left subclavian artery revascularization: Society for Vascular Surgery Practice Guidelines. J Vasc Surg 2010; 52: 65S–70S. 3. Czerny M, Eggebrecht H, Sodeck G, et al. Mechanisms of symptomatic spinal cord ischemia after TEVAR: insights from the European Registry of Endovascular Aortic Repair Complications (EuREC). J Endovasc Ther 2012; 19: 37–43.
Downloaded from vas.sagepub.com at University of Otago Library on October 11, 2015
Case Report
An unusual cause of spinal cord ischemia after thoracic endovascular repair
Vascular 0(0) 1–3 ! The Author(s) 2015 Reprints and permissions: sagepub.co.uk/journalsPermissions.nav DOI: 10.1177/1708538114565694 vas.sagepub.com
Issam Koleilat, Erin Moore, Tod Hanover and John Eidt
Abstract A 59-year-old left-handed man presented with chest pain and hypertension and was found to have an acute descending aortic dissection on imaging. After thoracic endovascular repair of the dissection, he developed left arm weakness and ischemia. Despite carotid-subclavian transposition, the patient was found to have persistent left triceps weakness as well as bilateral leg paresis. An urgent spinal drain was placed that improved his lower extremity deficit but did not greatly change his arm symptoms. Magnetic resonance imaging of the spine revealed previously undiagnosed severe multilevel spinal stenosis requiring operative decompression. To our knowledge, this is the first report of the contribution of cervical spinal stenosis to post-thoracic endovascular repair spinal ischemia.
Keywords Aortic dissection, TEVAR, spinal ischemia
Case A 59-year-old left-handed man presented with chest pain and hypertension. He reported cocaine use prior to presentation. He was employed as a landscaper. Imaging revealed a focal acute Type B aortic dissection confined to the proximal descending thoracic aorta. Despite aggressive blood pressure control, his pain persisted and he was offered thoracic endograft repair (TEVAR). He underwent placement of a 32 mm 120 mm Zenith TX2 endograft (Cook Medical) with partial coverage of the left subclavian artery using intravascular ultrasound (IVUS) and fluoroscopy (Figure 1) demonstrating complete occlusion of the false lumen. On postoperative day 1, he developed new onset left hand paresthesias and pain with loss of the left radial pulse. He also complained of bilateral leg and left arm weakness. He was taken to the operating room urgently for left carotid subclavian transposition. Postoperatively, he was found to have bilateral leg paresis. A spinal drain was placed and cerebrospinal fluid (CSF) was removed to reach a CSF pressure of 10 mmHg. His lower extremity paresis resolved completely over the next 12 h, and while his left arm symptoms improved overall, his weakness of the left triceps persisted. Magnetic resonance imaging (MRI) of the spine revealed severe multilevel disease with large disk protrusion and severe spinal stenosis at C3-7 with central
cord ischemia (Figure 2). Additionally, there was posterior central disk protrusion at L3-5. The patient underwent C3-7 laminoplasty with arch fixation. His residual left arm weakness slowly improved over several weeks of rehabilitation.
Discussion To our knowledge, this is the first report of cervical spinal stenosis contributing to post-TEVAR spinal ischemia associated with coverage of the left subclavian artery. We hypothesize that this patient had delayed thrombosis of his subclavian artery leading to ischemia in two vascular beds: the left arm as well as the cervical spinal cord. We believe that his left arm symptoms resulted from a combination of upper extremity arterial insufficiency as well as cervical cord ischemia. His cervical spondylosis with focal segmental spondylolithesis resulted in multilevel severe spinal stenosis that likely increased the vulnerability of the cervical cord to vascular injury. The patient’s spinal cord was Department of Vascular Surgery, Greenville Health Systems, Greenville, USA Corresponding author: Issam Koleilat, Greenville Health System, 701 Grove Road, Greenville, SC 29605, USA. Email: [email protected]
Downloaded from vas.sagepub.com at University of Otago Library on October 11, 2015
2
Vascular 0(0)
Figure 1. Angiogram depicting focal aortic dissection (left). Excluded dissection with partial coverage of the left subclavian artery (right).
Figure 2. Cervical MRI demonstrating severe cervical spondylosis with focal segmental spondylolithesis resulting in severe spinal stenosis of C3-7. MRI, magnetic resonance imaging.
compromised due the ‘‘pincer effect’’: compression by a hypertrophied ligamentum flavum posteriorly and protruding calcified disc anteriorly. As a result of the cord’s compromised physiology, it was particularly sensitive to further insults, both ischemic and compressive. Thus, the spinal cord edema from ischemia may have
been asymptomatic, but there was significantly reduced space in the spinal canal due to the undiagnosed spinal stenosis. While impossible to prove, we suspect that the ischemic insult was indirectly magnified by the presence of spinal compression. This vulnerability to ischemic injury has not been quantified in the literature, but is widely accepted theoretically. To date there are no reports of spinal cord ischemia after TEVAR exacerbated by cervical spinal stenosis. Currently described risk factors include coverage length (especially greater than 200 millimeters), coverage of T8-T12 intercostal vessels, prior abdominal aortic aneurysm repair, postoperative hypotension and left subclavian artery coverage.1,2 More recent data indicate that coverage of at least two of the four vascular territories that supply the spinal cord (left subclavian, intercostal, lumbar and hypogastric arteries) are needed to produce symptomatic spinal ischemia.3 We therefore suggest that preexisting severe spinal cord compression may additionally predispose patients undergoing TEVAR to spinal cord ischemia. In summary, it is likely that cervical spinal stenosis increases the vulnerability of the spinal cord to ischemic injury. In the setting of significant cervical spinal stenosis, we recommend prophylactic revascularization of the left subclavian artery prior to planned coverage during TEVAR.
Patient consent The patient described herein had given consent to the use of deidentified patient data for use in research and education as per institutional policy.
Downloaded from vas.sagepub.com at University of Otago Library on October 11, 2015
Koleilat et al.
3
Conflict of interest None declared.
Funding This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors.
References 1. Buth J, Harris PL, Hobo R, et al. Neurologic complications associated with endovascular repair of thoracic aortic pathology: Incidence and risk factors. A study from the
European Collaborators on Stent/Graft Techniques for Aortic Aneurysm Repair (EUROSTAR) registry. J Vasc Surg 2007; 46: 1103–10. (discussion 10–1). 2. Matsumura JS and Rizvi AZ. Left subclavian artery revascularization: Society for Vascular Surgery Practice Guidelines. J Vasc Surg 2010; 52: 65S–70S. 3. Czerny M, Eggebrecht H, Sodeck G, et al. Mechanisms of symptomatic spinal cord ischemia after TEVAR: insights from the European Registry of Endovascular Aortic Repair Complications (EuREC). J Endovasc Ther 2012; 19: 37–43.
Downloaded from vas.sagepub.com at University of Otago Library on October 11, 2015
