Ann Thorac Surg 2007;84:1738-1740. doi:10.1016/j.athoracsur.2007.05.076
© 2007 The Society of Thoracic Surgeons
Case Reports
Three Cases of Newly Developed Paraplegia After Repairing Type A Acute Aortic Dissection
Yujiro Kawanishi, MD,
Kenji Okada, MD,
Keitaro Nakagiri, MD,
Atsushi Kitagawa, MD,
Hiroshi Tanaka, MD,
Masamichi Matsumori, MD,
Yutaka Okita, MD*
Division of Cardiovascular, Thoracic, and Pediatric Surgery, Kobe University Graduate School of Medicine, Kobe, Japan
Accepted for publication May 30, 2007.
* Address correspondence to Dr Okita, 7-5-2, Kusunoki-cho, Chuo-ku, Kobe City, Hyogo, 650-0017, Japan (Email: yokita{at}med.kobe-u.ac.jp).
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Abstract
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Postoperative paraplegia after repairing type A acute aortic dissection has been rarely reported and the causes have not been clearly elucidated. We had three cases of newly developed paraplegia after repair of type A acute aortic dissection. In these cases, we speculated that some intercostal arteries were occluded by completely thrombosed false lumen with late onset of systemic hypotension, which might have reduced spinal cord perfusion followed by paraplegia.
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Introduction
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Although paraplegia is well known as a complication after thoracoabdominal aortic repair [1], postoperative paraplegia after repair of type A acute aortic dissection has rarely been reported [2, 3]. We present three cases of newly developed paraplegia after repair of type A acute aortic dissection.
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Case Reports
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Patient 1
A 51-year-old man with acute type A aortic dissection underwent total arch replacement. He had regained consciousness and strength of his extremities, but 2 hours after extubation, weakness of his lower extremities had developed and progressed to paraplegia. His mean arterial pressure was approximately 70 mm Hg. A chest computed tomographic scan demonstrated that false lumen of the descending thoracic aorta was completely thrombosed (Fig 1). A cerebrospinal fluid (CSF) catheter was immediately inserted. Initial CSF pressure was 28 mm Hg and drainage was continued for 3 days to maintain the CSF pressure below 10 mm Hg. At the same time, the mean arterial pressure was augmented up to 100 mm Hg with dopamine and dobutamine to maintain adequate spinal perfusion pressure. Corticosteroid, free radical scavenger, and mannitol were administered as well. Paraplegia was fully recovered promptly.
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Fig 1. Postoperative chest computed tomographic scan demonstrates that false lumen of the descending aorta is completely thrombosed.
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Patient 2
A 54-year-old man with severe mitral insufficiency underwent valve repair. Type A aortic dissection originating from the aortic cannulation site was found intraoperatively, and ascending aortic repair was performed. He regained consciousness with normal movement of extremities. However, on day 2, his systolic blood pressure deteriorated down to 50 mm Hg because of cardiac tamponade. After re-exploration for bleeding, he regained consciousness with weakness of the lower extremities. Angiography demonstrated that the false lumen of the descending thoracic aorta was completely thrombosed and the intercostal arteries originating from the false lumen were occluded. Systolic arterial pressure augmentation with dopamine and CSF drainage was performed for 3 days, and mannitol and corticosteroid were used. Leg movement recovered gradually and eventually he could walk independently.
Patient 3
A 57-year-old man with acute type A aortic dissection underwent total arch replacement. He recovered without any neurologic complications. Twenty-four hours after the operation, he suddenly collapsed due to cardiac tamponade with decreased systolic blood pressure down to 40 mm Hg, and he was re-explored for bleeding. He regained consciousness presenting with paraplegia. A computed tomographic scan demonstrated that the false lumen of the descending thoracic aorta was thrombosed. Magnetic resonance imaging revealed spinal cord infarction at the level between Th6 and L2 (Fig 2). The arterial mean pressure was maintained over 90 mm Hg with dopamine, but the CSF drainage was not applied because 24 hours had passed after diagnosis of spinal cord infarction. He was discharged with permanent neurologic deficit.
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Fig 2. The T2-weighted magnetic resonance imaging shows high signals in the spinal cord, which indicates spinal cord infarction (white arrows).
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Comment
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Postoperative hypotension and increased CSF pressure are reported to be potential causes of delayed paraplegia after thoracoabdominal aortic repair [4, 5]. However, the causes of paraplegia after repairing type A aortic dissection have not been clearly elucidated. In our cases, chest computed tomographic or angiographic scans had demonstrated that the false lumen of the dissected aorta was completely thrombosed. More importantly, postoperative hypotension occurred in 2 patients. We speculated that thrombosed false lumen occluded some intercostal arteries and reduced spinal cord perfusion, which resulted in paraplegia in patient 1. In patients 2 and 3, spinal cord perfusion was maintained just after the aortic repair, even when the false lumen had been thrombosed, but late onset of systemic hypotension reduced spinal cord perfusion and led to paraplegia.
Another possible cause of paraplegia is deep hypothermic circulatory arrest of the lower body during operation. However, the majority of our 163 patients who underwent total arch replacement under deep hypothermic circulatory arrest for thoracic aortic aneurysm did not have postoperative paraplegia, although circulatory arrest time was comparable with these 3 patients. Circulatory arrest does not seem to be the cause of paraplegia in our cases.
Because CSF drainage and augmentation of arterial pressure have been reported to be effective to counteract the delayed paraplegia after open surgery or endovascular repair [4, 5], we have applied them with medications such as corticosteroid, free radical scavenger, and mannitol. To maintain appropriate spinal cord circulation, the systemic mean arterial pressure should be greater than 100 mm Hg and the CSF pressure should be below 10 mm Hg, respectively. We believe that such interventions are useful in the case of paraplegia after repairing type A acute aortic dissection.
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References
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- Safi HJ, Estrera AL, Miller CC, et al. Evolution of risk for neurologic deficit after descending and thoracoabdominal aortic repair Ann Thorac Surg 2005;80:2173-2179.
- DeBakey ME, McCollum CH, Crawford ES, et al. Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically Surgery 1982;92:1118-1134.
- Medalion B, Bder O, Cohen AJ, Hauptman E, Schachner A. Delayed postoperative paraplegia complicating repair of type A dissection Ann Thorac Surg 2001;72:1389-1391.
- Cheung AT, Weiss SJ, McGarvey ML, et al. Interventions for reversing delayed-onset postoperative paraplegia after thoracic aortic reconstruction Ann Thorac Surg 2002;74:413-421.
- Cheung AT, Pochettino A, McGarvey ML, et al. Strategies to manage paraplegia risk after endovascular stent repair of descending thoracic aortic aneurysms Ann Thorac Surg 2005;80:1280-1289.
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Abstract
Introduction
