Anterior Spinal Artexy Syndrome with Chronic Traumatic Thoracic Aortic Aneurysm Vincent R. Conti, M.D., John Calverley, M.D., William L. Safley, M.D., Melinda Estes, M.D., and Edward H. Williams, M.D. ABSTRACT Shortly after severe blunt chest trauma, a young man experienced neurological symptoms suggestive of a spinal cord lesion at the lower thoracic level. The symptoms resolved at first, but then recurred 3 years later and progressed slowly. Neurological workup failed to define the cause until a thoracic aortogram showed an aneurysm in the middle portion of the descending aorta in close proximity to a vessel supplying the anterior spinal artery. After the operative repair with precautions taken to avoid further neurological injury, the neurological deficit resolved partially. Because of the potential for symptomatic spinal cord ischemia resulting from lesions of the aorta, angiographic delineation of the spinal cord blood supply is valuable in planning operative repair. When ischemic injury to the spinal cord occurs after aortic disruption from blunt chest trauma, the cause is nearly always inadequate blood flow to the spinal cord during operative repair, and the result is usually paraplegia. The risk of this tragic perioperative complication is well known for all types of aneurysms involving the thoracic and the abdominal aorta [l-91. However, neither surgeons nor neurologists have recognized the potential for the occurrence of lesser degrees of symptomatic spinal cord ischemia before operative intervention and due solely to an aneurysm close to a major vessel supplying the anterior spinal artery. This report presents the case of a patient who first experienced an unusual neurological deficit shortly after severe chest trauma and, 5 years later, was found to have a chronic traumatic aneurysm in the middle portion of the descending aorta. From the Department of Surgery, Division of Cardiothoracic Surgery, and the Department of Neurology, The University of Texas Medical Branch, Galveston, TX. Accepted for publication Jan 8, 1981. Address reprint requests to Dr. Conti, Division of Cardiothoracic Surgery, The University of Texas Medical Branch, Galveston, TX 77550. After operative repair with special precautions taken to avoid further neurological damage, the patient unexpectedly experienced an unequivocal, albeit partial, resolution of the neurological deficit. A 27-year-old man was referred to the Neurology Service of the University of Texas Medical Branch at Galveston for evaluation of a sensory deficit in both lower extremities, low thoracic back pain, and bilateral leg pain. Several years earlier, in August, 1975, an automobile accident had caused considerable blunt injury to the chest with sternal and rib fractures; the patient had been unconscious for a brief period. He recovered and was discharged from the hospital ten days after the injury with no neurological deficit evident to himself or his physicians. A week after discharge, however, he noticed a decrease in pain and in temperature sensation in the lower extremities. He was rehospitalized and a myelogram of the lumbar and thoracic regions was interpreted as normal. Over the next 3 months, the neurological symptoms resolved gradually, and he returned to work as an oil driller in December, 1975. He was well until February, 1979, when he felt "something snap" in his back as he was pulling an oil drilling collar. The same sensory deficit that had occurred in 1975 returned, this time accompanied by pain in the region of the lower thoracic vertebrae, and pain and weakness in both legs. These symptoms progressed gradually over the next year or so, such that he could no longer perform the strenuous work required by his employment. Another myelogram was performed, which was interpreted as normal, and he was referred to us for evaluation. Neurological examination on admission in May, 1980, demonstrated loss of temperature sensation and greatly decreased pain sensation in both lower extremities, with an ill-defined 81 0003-4975/82/010081-05$01.25 @ 1980 by The Society of Thoracic Surgeons
82 The Annals of Thoracic Surgery Vol 33 No 1 January 1982 sensory level at the tenth or eleventh thoracic level (T-10 or T-11) and weakness of the dorsiflexors and plantarflexors of the toes bilaterally. He had moderately severe pain centered over the T-8 to T-10 vertebrae with paravertebral muscle spasm and local tenderness to palpation. Lower extremity pulses were normal. A repeat myelogram was interpreted as normal; the only reservation was a suggestion of abnormal vessels that might indicate an arteriovenous malformation. Findings on a computed tomographic scan of the spinal cord were normal. Results of peripheral nerve conduction studies were normal, and an electromyogram showed changes in the right anterior tibia1 muscle group indicative of denervation. Because of the findings on the myelogram, a thoracic aortic angiogram was done, with selective injections to demonstrate the blood supply to the spinal cord. This study disclosed an aneurysm in the middle portion of the descending thoracic aorta from T-6 to T-8 (Fig 1). Selective injections demonstrated a vessel from the intercostal artery at T-9, with anastomotic connections to the T-8 and T-10 intercostals that supplied the anterior spinal artery (Fig 2). This was interpreted as representing the arteria radicularis magna. An operation was performed to repair the aneurysm. Because of the possibility of temporary interruption of circulation to the arteria radicularis magna during the repair, thoracotomy was preceded by externally induced total-body hypothermia (to 31 C) and phlebotomy-induced mild hemodilution, with retransfusion of autologous blood later in the operation. A posterolateral thoracotomy incision was used, the sixth rib was resected, and the anterior and lateral extent of the aneurysm was dissected free. A 9 mm heparin-coated shunt was inserted above and below the aneurysm, which was opened longitudinally. After the interior of the aneurysm was inspected, the distal clamp was placed in an angled fashion to maintain blood flow to the T-9 intercostal artery. The aneurysm was smooth and thin walled; there was no clot or debris. No vessels originated from the involved segment, although the T-8 intercostal artery originated just at the Fig 1. Anteroposterior view of the thoracic aortogram showing an aneurysm extending from T-6 to T-8. lower lip of normal aorta where it met the thin aneurysm wall. The aneurysm appeared to have resulted from a circumferential traumatic disruption of the aorta, and the proximal and distal ends of the aneurysm represented the two separated ends of the torn aorta. To suture the Dacron tube graft into place, the intercostal artery originating at T-8 had to be occluded in the distal suture line. At the close of the procedure, the patient was rewarmed. After the operation, the patient experienced a return of temperature sensation and clear improvement in pain sensation in the lower extremities. The back and leg pain was absent at first; it returned later in his convalescence, but was mild. A neurological examination eight days after operation, and one performed 2 months postoperatively, confirmed the substantial although incomplete reduction of the pain and sensory deficit below T-10. Motor function of the lower extremities had improved, and subjective amelioration of the back and leg pain was clear.
83 Case Report: Conti et al: Anterior Spinal Artery Syndrome A B Fig 2. (A) Opacification of T-8 and T-9 intercostal arteries on a delayed angiogram after selective injection of the T-I0 intercostal artery (no longer filled). There is an anastomotic network connecting these intercostals and an ascending vessel, the arteria radicularis magna, originating at T-9 and filling the anterior spinal artery (arrows). (B) Line interpretation of angiographic findings. Comment Before an angiographic study unexpectedly demonstrated an aneurysm of the middle portion of the descending thoracic aorta just proximal to the arteria radicularis magna, this young, vigorous man was thought to suffer from a primary intrinsic spinal cord lesion such as a tumor, arteriovenous malformation, or syringomyelia. In retrospect, however, this finding permitted recognition that the severe blunt chest trauma had disrupted the aorta in an area that could affect spinal cord blood supply. Soon after injury, he experienced symptoms typical of a central cord lesion, which re- solved gradually over the next 3 months, only to recur 3 years later when progression of the neurological deficit then led to further study. Preoperative arteriograms with selective injections into the intercostal arteries detailed the blood supply to the anterior spinal artery from the intercostals just below the aneurysm, thus providing information that minimized the danger of intraoperative spinal cord ischemia and permanent neurological injury. The fact that the patient s neurological deficit occurred shortly after the severe chest trauma that caused the aortic disruption and resolved partially after repair of the aneurysm is convincing evidence that the aneurysm in some way compromised spinal cord blood supply. We can only speculate on the exact mechanism, but it is possible that the aneurysm caused spatial distortion or compression of the vessels that give rise to the arteria radicularis magna. It is also possible that the prominent ridge of tissue at the lower margin of the aneurysm posteriorly
84 The Annals of Thoracic Surgery Vol 33 No 1 January 1982 caused an altered blood flow pattern just distal to it where the arteria radicularis magna originated. In a similar case reported in 1980, the traumatic aneurysm involved the lower portion of the descending thoracic aorta, and selective arteriography identified a vessel originating at the proximal margin of the aneurysm that supplied the anterior spinal artery [lo]. Since this aneurysm was small and asymptomatic and since repair would carry a high risk of paraplegia, the surgeons elected not to repair it, but rather to follow it with periodic noninvasive studies. Although the management of chronic traumatic aortic aneurysms has been a subject of controversy, the accumulated data suggest that expansion occurs later in as many as a third of patients 111, 121 and that rupture may happen even years later without warning. As a consequence, most surgeons advocate operative repair in patients who are otherwise good risks. Our patient s persistent back pain centered over the level of the aneurysm, and the slowly progressing neurological deficit provided further compelling indications for repair. Spinal cord lesions, progressing from transient minor sensory and motor deficits to permanent paraplegia, have been reported to occur spontaneously with acute dissecting aortic aneurysms [5, 71 and with ruptured atherosclerotic aortic aneurysms [7, 131. With dissecting aneurysms, vessels that supply the cord may be occluded suddenly as the dissecting process extends to the descending aorta; with ruptured atherosclerotic aneurysms, severe hypotension may further compromise the already marginal blood supply to the cord. Atherosclerotic and dissecting aneurysms might be expected to cause such lesions more frequently, as they regularly involve the aorta from T-8 to the fourth lumbar level where the arteria radicularis magna originates, whereas traumatic disruptions usually involve the thoracic aorta just distal to the left subclavian artery and well proximal to the arteria radicularis magna. Paraplegia has occurred, however, shortly after traumatic aortic transection in this location, and before operation was undertaken. In 3 patients [14-161 it was a con- sequence of acute aortic occlusion at the site of the tear and, in another 3 [17, 181, probably a consequence of extrinsic compression and occlusion of intercostal arteries by periaortic hematoma. When traumatic disruptions occur in the more distal descending thoracic aorta, the site is usually at the point of aortic fixation at the diaphragm, but may also be in the middle part of the descending thoracic aorta, as in the patient presented here. Because of the anatomy of the blood supply to the spinal cord, these lesions might be expected to have a higher risk of seriously compromising the blood supply by impingement on the arteria radicularis magna. Because of the variability of blood supply to the thoracic and lumbar areas of the spinal cord, it is impossible to predict whether an aneurysm at any specific level may cause cord ischemia. When the arteria radicularis magna originates above the renal arteries, it usually represents the only major thoracolumbar radicular branch, but when its origin is infrarenal, there is usually another major radicular branch in the middle or lower thoracic area [191. This unpredictability of vascular supply to the spinal cord suggests that in some patients with aneurysms, special studies to define the anatomy of the blood supply to the anterior spinal artery might be valuable in avoiding perioperative paraplegia. Although these studies carry a small but definite risk of spinal cord injury, the procedure is safe when properly performed, and the risk is minimal. Had we not known the exact location of the arteria radicularis magna, which, in our patient, arose barely 2 cm below the lower lip of the aneurysm, special precautions might not have been taken and paraplegia might well have resulted. Although it was unique, the case described here demonstrates that a relatively mild spinal cord lesion that is manifest after blunt chest trauma may be due to traumatic disruption of the aorta and that the deficits may be at least partially reversible with repair. It illustrates further how precarious the spinal cord blood supply may be and emphasizes the value of precise delineation of its anatomy by selective angiography in planning the details of operative repair.
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