Acute spinal cord ischemia during aortography.

To the Editor: We read with utmost interest the report from Restrepo and Guttin1 that described a case of acute spinal cord ischemia, which resulted from aortography in a patient with severe systemic atherosclerosis. In their patient, the injury occurred during apparently straightforward aortography for the evaluation of an aneurysm of the abdominal aorta. The patient was successfully treated with intravenous recombinant tissue plasminogen activator within 3 hours after the onset of symptoms, and he was discharged 3 days after thrombolysis, able to walk unassisted. We had a 79-year-old patient with recent-onset angina pectoris, severe aortic and systemic atherosclerotic disease, and chronic moderate renal failure, who developed extensive spinal cord ischemia after a much more demanding right femoral coronary angiography, because of severe full-length aortic and iliac tortuosity. Our case was never reported in the literature, but it was presented and discussed during some meetings in Europe.2 We were forced to use a 45-cm-long 6F introducer, ultra-stiff 0.35-inch Amplatz exchange wires (Cook Medical Inc.; Bloomington, Ind), and 6F coronary angioplasty catheters in order to opacify the coronary tree. Moderately severe disease of the right coronary and left circumflex arteries, suitable for coronary angioplasty, was discovered. We did not proceed, because the patient had dull back pain and felt exhausted despite the fact that the procedure did not last too long (29 minutes), considering the technical difficulties that we had faced. When we moved him from the catheterization table to the stretcher, we realized that he had complete flaccid paralysis of the legs associated with sensory loss, and a livedo reticularis extending from the umbilical line to the feet. The femoral pulses were brisk. We hypothesized that there had been a plaque dislodgement, with embolization of a costal artery that supplied the spinal cord, caused by the long sheath or by passage of the stiff wires or catheters. In the hope that some fresh, platelet-rich thrombi were present with the chronic plaque material and cholesterol crystals, we decided to inject a fullbolus (180 μg/kg) and a half bolus (90 μg/kg) 10 minutes apart, instead of 2 full boli (because of the patient's age and renal failure), followed by a continuous infusion of 2.0 μg/kg per min for 12 hours. Low doses of dopamine, nitroprusside, and pentoxifylline were also given. Soon afterwards, the patient underwent emergency computed tomographic scanning and intravenous aortography, which ruled out an aortic dissection. Some 40 minutes after the end of the last eptifibatide bolus, the patient started moving his legs, with gradual recovery of his sensory function and regression of the livedo. It took some days for him to walk unassisted. His renal function deteriorated (creatinine level from 3.5 up to 4.5 mg/dL), but that reversed in a matter of 3 weeks. The diagnosis of spinal cord injury was confirmed by the neurologist on duty and also by nuclear magnetic resonance imaging 1 week after the procedure. The patient was discharged from the hospital, asymptomatic for angina, on medical treatment, and he has been well since then. The occurrence of spinal cord ischemia during angiography is a very serious matter. Excluding the 2 cases discussed here,1,2 5 have been described in the English literature since 1972—4 occurring during aortography and 1 during coronary angiography.3 Our colleagues have shown us that this dreadful complication can be treated successfully with antithrombotic drugs,1 without hemorrhage in the spinal cord. The 2 types of drugs are probably both effective: IIb/IIIa glycoprotein inhibitors may be preferred if they are used, as in our present case, immediately after the insult, when the presence of a white thrombus is more likely. The therapeutic window for thrombolytic agents is probably wider. It would be interesting to know whether these drugs can be successfully used in at least some cases of acute spinal ischemia observed after the percutaneous implantation of an aortic prosthesis, or even after thoracoabdominal aortic surgery. In this last situation, the potential benefit might be obscured by the risk of serious bleeding from the sutures. Perhaps lower-dose local therapy could be given, for a lower risk of hemorrhage. Vito Paolillo, MD Daniela Gastaldo, MD Cardiac Interventional Unit, San Giovanni Bosco Hospital, Turin, Italy