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Ann Thorac Surg 2002;73:1971-1973
© 2002 The Society of Thoracic Surgeons
a Heart Center, John Radcliffe Hospital, Headington, Oxford, United Kingdom
Accepted for publication December 5, 2001.
* Address reprint requests to Dr Geyer, 1 St. Mary’s Way, Guildford, Surrey GU2 8JY United Kingdom
e-mail: tomy{at}gohip.com
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Introduction |
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A 65-year-old male with ischemic heart disease underwent elective coronary artery bypass grafting. He suffered from end-stage renal failure caused by hypertensive nephropathy for which he was on continuous ambulatory peritoneal dialysis. Apart from bronchial asthma, which was treated with inhalers, there was no history of any other relevant medical illnesses such as peripheral vascular disease, spinal problems, or cerebrovascular disease. He underwent triple coronary artery bypass grafting in which the left internal mammary artery was anastomosed to the left anterior descending coronary artery, and reversed long saphenous vein graft was fashioned to the first obtuse marginal and the right coronary artery. A technique of intermittent cross-clamp fibrillation was used. Clinically the ascending aorta was normal to palpation and did not show signs of significant plaque disease.
The postoperative period was uneventful and the patient was extubated within 4 hours of the operation. Though there was no urine output because of the renal failure, the patient appeared well perfused and was never acidotic. On the morning after the operation, he started to complain of inability to move both lower limbs. Neurologic examination revealed an alert and orientated patient with established motor weakness of both lower limbs. The sensory component was partially intact with the patient responding to touch, pain, and temperature. The deep tendon reflexes and the plantar reflexes were absent. Anal sphincter tone and reflexes were abolished.
There was no clinical evidence of a cerebrovascular accident or aortic dissection. Values for protein C and protein S were in the normal range. A magnetic resonance imaging scan was performed which showed a central high signal in the lumbar cord (Figs 1 and 2). The features were consistent with an area of spinal cord infarction in the distribution of the anterior spinal artery, or artery of Adamkiewicz. There was no visible dissection or unstable plaque seen in the descending aorta. The patient is under regular follow-up and undergoing rehabilitation with no features of recovery in motor power.
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Comment |
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Isolated CABG complicated by spinal infarction without the use of an intraaortic balloon pump (IABP) or aortic dissection is exceptional [2]. Gottesman and colleagues [3] reported 8 patients after CABG, all of whom were associated with the use of an IABP. It is more commonly associated with repairs of descending thoracic aneurysms and less frequently with other aortic procedures such as aortic dissections [2, 4]. All other cases reported after cardiac procedures including CABG have been associated with the use of an intraaortic balloon pump [3, 5, 6]. Nevertheless, one patient reported by Thomas and colleagues [2] underwent CABG as an emergency operation shortly after an acute inferior wall infarction and had paraplegia develop postoperatively. This patient suffered from severe aorto-iliac occlusive disease. Most patients had bilateral leg weakness develop, but modified Brown-Séquard syndrome has been described [3].
The mechanisms of spinal cord injury are various, but the most plausible causes are microembolization of atherosclerotic plaques or cholesterol emboli. In cases of spinal infarction in which an intraaortic balloon pump has been used, the causing mechanism seems to result from plaque embolization from aortic atheromas. Where no IABP has been used the mechanism is less clear. Short episodes of severe hypertension causing embolization or cross clamping of the aorta as a reason for embolization have been discussed in the literature [2].
Hypotension and hypoperfusion leading to infarcts in watershed areas are also recognized [2, 3, 5]. In particular, the lower spinal cord is susceptible to systemic hypotension because of the lack of collateral blood supply. Conditions such as protein C or protein S deficiency can contribute or increase the risk of having thromboembolic events develop [5]. Spinal ischemia from dissection of the aorta starting from the cannulation site or the top-end anastomotic site should also be considered.
Only Harris and colleagues [5] have provided pathologic evidence of the underlying event (embolization or hypotension) in which cholesterol microemboli were found in the radicular arteries. An IABP was used in their patient; nevertheless, trauma such as intimal laceration or medial dissection of the aorta was not found. The origin of these emboli is most likely the aorta, which is manipulated during cross clamping or insertion of the IABP. Otherwise a clear cause for spinal infarction after CABG with or without the insertion of an IABP has not been established in the literature. Thomas and colleagues [2] postulated a hypertensive crisis with dislodgement of atheromatous plaques from a calcified aorta as the potential cause of spinal infarction. However, in one of their two cases an IABP was inserted. Therefore the cause of plaque dislodgement and embolization could have been caused by the IABP. None of the previous reports in the literature supports the view that a hypertensive crisis is responsible for this. It is generally agreed that peripheral vascular disease is a significant risk factor for perioperative stroke syndromes. The literature supports the view that hypotension is more detrimental to spinal cord perfusion, and short episodes of hypertension are generally well tolerated especially in hypertensive patients [3, 5].
A balloon pump was not used in our patient, and there was no aortic dissection. The patient did not suffer from peripheral vascular disease, and there was not any evidence of thrombophilia. There were no excessive swings in perioperative blood pressure. The aorta was manipulated during intermittent cross clamping, but the cause of the selective embolization to the anterior spinal artery is not clear.
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  C. E. Robertson, R. D. Brown Jr, E. F. M. Wijdicks, and A. A. Rabinstein Recovery after spinal cord infarcts: Long-term outcome in 115 patients Neurology, January 10, 2012; 78(2): 114 - 121. [Abstract] [Full Text] [PDF]
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 P. M. Spielmann and C. Campanella Spinal infarction following coronary artery bypass grafting Interact CardioVasc Thorac Surg, December 1, 2004; 3(4): 606 - 607. [Abstract] [Full Text] [PDF]
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