Asian Cardiovasc Thorac Ann 2007;15:255-257
© 2007 Asia Publishing EXchange Ltd
Coincidence of Spinal Canal Stenosis and Thoracoabdominal Aortic Aneurysm
Justin James, FRCS Ed,
Manoj Kuduvalli, FRCS,
John Y Lu, FRCS,
Abbas Rashid, FRCS
The Cardiothoracic Centre NHS Trust, Liverpool, United Kingdom
For reprint information contact: Justin James, FRCS Ed, Tel: 44 151 228 1616, Fax: 44 151 724 1954, Email: drjustinjamesj{at}yahoo.co.uk, Cardiothoracic Surgery, The Cardiothoracic Centre, Thomas drive, Liverpool L14 3PE, United Kingdom.
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ABSTRACT
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We report a case in which a thoracoabdominal aneurysm was present in association with previously unknown critical spinal canal stenosis. In spite of using left heart bypass, systemic hypothermia, and controlled cerebrospinal fluid drainage for spinal cord protection, the patient developed paraplegia following aortic aneurysm repair. Computed tomography scan revealed critical stenosis of the spinal canal that was thought to be sufficient to produce spinal cord compression syndromes including paraplegia.
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INTRODUCTION
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Spinal cord injury resulting in neurological deficit is a devastating complication following surgical repair of thoracoabdominal aortic aneurysms. Underlying spinal cord abnormalities may make spinal cord vulnerable to ischemic insults. Identification of these abnormalities can help preventing neurological damage.
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CASE REPORT
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Mr L, a 53-year-old healthy non-smoker sustained an acute type A dissection of the aorta in March 2000, for which he underwent an urgent operation with interposition graft replacement of the ascending aorta and hemi arch. He made an uneventful recovery from this operation. Computed tomography (CT) scan performed 17 months after surgery at regular follow-up showed a non-expanding Extent II thoracoabdominal chronic dissecting aneurysm (an aneurysm that begins at the left subclavian artery and reaches the infrarenal abdominal aorta). The aneurysm began to expand 44 months after the initial surgery, with the descending thoracic aorta measuring 7 cm just distal to the left subclavian artery. The intimal flap that spiralled down the descending thoracic aorta through the abdominal aorta into the right common iliac artery was clearly visible on both CT (Figure 1A
) and magnetic resonance (MR) scan. The superior mesenteric, celiac, and right renal arteries arose from the true lumen. The left renal artery arose from the false lumen and was devoid of flow. The left kidney was atrophic.
The thoracoabdominal aortic aneurysm (TAAA) was electively repaired. Left heart bypass, mild systemic hypothermia, and controlled cerebrospinal fluid (CSF) drainage were used for spinal cord protection. The aneurysm was the largest just distal to the left subclavian artery and contained clots throughout its length. All intercostal arteries, some originating from true lumen and some from false lumen, were small except for two relatively large pairs close to the celiac artery. Using a sequential clamp technique, the thoracoabdominal aorta was reconstructed using a dacron tube graft (Hemashield Dacron Platinum; Boston Scientific Inc., Natick, MA, USA). The left renal vein and artery were tied off. The island of aorta bearing the origins of the right renal, superior mesenteric, celiac, and two pairs of intercostal arteries was mobilized and anastomosed to the graft as a patch. Controlled CSF drainage using a lumbar CSF catheter was used throughout the procedure to maintain CSF pressure less than 12 mm Hg.
The patient had a period of postoperative acute renal failure, which was managed conservatively. He was electively ventilated for three days. However, on the 4th postoperative day when he was weaned off the ventilator, fl accid paraplegia became evident. Computed tomography scan of the spine (Figure 1B) revealed marked posterior osteophyte formation at the T11/12 level causing spinal canal stenosis. The spinal canal was narrowed to 30% of the normal. The patient made a slow but steady postoperative recovery except for the neurological deficit, and was discharged to the neuro-rehabilitation centre 48 days after his operation.
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DISCUSSION
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Paraplegia is still a devastating complication that occurs in 5–40% of patients undergoing TAAA repair. Interference with spinal cord perfusion is generally accepted as the cause for paraplegia.1 As a result of such a frequent association between this complication and TAAA surgery, and also because of general acceptance of ischemia as the cause for this complication, these incidences are generally not investigated for other possible etiologies. Biglioli2 reported a case of paraplegia that developed due to extrinsic spinal cord compression by a hematoma following TAAA repair. Neurological deficit in acute spinal cord compression as in burst fractures is related to the degree of narrowing of the spinal canal.3 However the degree of narrowing in the thoracic spine that can produce paraplegia in its own right in degenerative conditions is variable. We believe that 70% spinal canal stenosis in this case contributed to the development of paraplegia.
The spinal cord depends on the anterior spinal artery for its blood supply. Segmental inputs from intercostal arteries are assumed to be essential for maintaining adequate flow in the anterior spinal artery.4 Spinal canal stenosis could compress the anterior spinal artery and block the flow between its proximal and distal parts concurrently, thereby increasing the perfusion pressure required to maintain tissue perfusion to the spinal cord at the level of the stenosis. The fall in spinal cord perfusion pressure following loss of many contributing segmental vessels and blocked anterior spinal artery could then easily tip the balance to drop the perfusion pressure below critical level at the level of the stenosis. Spinal cord compression could thus effectively act as a factor which could move the "ischemic time versus deficit curve" to the left in the conceptual model introduced by Svensson and Loop.5
Tissue edema that follows reversible ischemia and reperfusion injury could further compromise tissue perfusion at the level of the stenosis. Extreme positioning during the perioperative period under anesthesia could have further contributed to paraplegia by direct compression of the spinal cord. Fujioka et al6 reported quadriplegia that occurred following coronary artery bypass grafting. This patient had cervical stenosis that was not known preoperatively. The authors suggest that neck extension during surgery might have aggravated an occult pre-existing cervical spinal canal stenosis to produce cervical injury.
It is generally agreed that interference with the blood supply to the spinal cord is the reason for the paraplegia.7 Even after strictly following various combinations of measures described for prevention of this catastrophic complication, paraplegia or paraparesis still occurs with a frequency of 5–40%.1 Therefore other contributing factors in the genesis of postoperative paraplegia should be considered. The coincidence illustrated in this report could be one such possible cause. There is no previously reported case of coincidence of spinal cord abnormality in paraplegia following TAAA repair in the medical literature. In a MR evaluation of postoperative neurological deficits in 24 patients Mawad et al8 did not find extrinsic compression as a contributing factor. There are suggestions in the literature that patients evaluated for symptoms of spinal canal stenosis often have associated abdominal aortic aneurysm. However the reverse has not been reported. Since pre-existing spinal canal or cord pathology can predispose to spinal cord injury in TAAA, we suggest that patients with Extent II TAAA should be screened for evidence of spinal canal and cord abnormalities prior to surgical repair whenever possible.
In conclusion, we report a case of TAAA with coincident critical spinal canal stenosis. Spinal pathology in this case is thought to have contributed to postoperative paraplegia. We suggest that patients with TAAA should be screened for spinal pathology since this can be done when they are evaluated for aortic disease.
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REFERENCES
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- Wan IY, Angelini GD, Bryan AJ, Ryder I, Underwood MJ. Prevention of spinal cord ischaemia during descending thoracic and thoracoabdominal aortic surgery. Eur J Cardiothorac Surg 2001;19:203–13.[Abstract/Free Full Text]
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- Svensson LG, Loop FD: Prevention of spinal cord ischemia in aortic surgery. In: Bergan JJ, Yao JST, editors. Arterial Surgery: New Diagnostic and Operative Techniques. New York: Grune & Stratton, 1988;273–85.
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ABSTRACT
INTRODUCTION
