Abstract
Objective: To evaluate the rate of spinal cord infarction after aortic repair.
Background: Spinal cord infarction accounts for 1% of all strokes but its rate after repair of an aortic aneurysm or dissection is uncertain.
Design/Methods: We performed a retrospective cohort study using administrative data from all inpatient discharges in California, Florida, and New York in the period 2005–2013. We included patients who underwent surgical or endovascular repair of a thoracic or abdominal aortic aneurysm or dissection. Our outcome variable was an incident diagnosis of spinal cord infarction (ICD9-CM codes: 336.1, 344.1–344.5, 344.9) occurring during the index hospitalization for aortic repair. Descriptive statistics with exact confidence intervals (CIs) were used to report crude rates of spinal cord infarction in patients with repair of an unruptured versus ruptured aortic aneurysm or dissection. In secondary analysis, we evaluated the rate of spinal cord infarction in these groups by treatment approach – surgical versus endovascular.
Results: We identified 90,506 patients who underwent repair for an aortic aneurysm or dissection, and spinal cord infarction was diagnosed in 618 cases (0.68%, 95% CI, 0.62–0.73%). In patients with ruptured aneurysm or dissection, the rate of spinal cord infarction was 2.02% (95% CI, 1.80–2.24%), compared to 0.40% (95% CI, 0.36–0.45%) in patients undergoing repair of an unruptured aneurysm. Among patients who underwent repair of a ruptured aneurysm or dissection, spinal cord infarction occurred in 1.96% (95% CI, 1.70–2.21%) of patients who had a surgery and in 2.18% (95% CI, 1.74–2.62%) of patients who had endovascular repair. Among those with an unruptured aneurysm, spinal cord infarction occurred in 0.58% (95% CI, 0.49–0.67%) of patients who received surgery and 0.29% (95% CI, 0.24–0.34%) of those who had endovascular repair.
Conclusions: The rate of spinal cord infarction after aortic repair is low overall, but is higher after repair of a ruptured aortic aneurysm or dissection.
Study Supported by:
Dr. Gialdini is supported by the Feil Family Foundation.
Dr. Kamel is supported by NIH grants K23NS082367 and R01NS097443 as well as the Michael Goldberg Research Fund.
Disclosure: Dr. Gialdini has nothing to disclose. Dr. Merkler has nothing to disclose. Dr. Parikh has nothing to disclose. Dr. Lerario has nothing to disclose. Dr. Chatterjee has nothing to disclose. Dr. Kamel has received personal compensation for activities with Genentech as a speaker. Dr. Kamel has received personal compensation in an editorial capacity for Journal Watch Neurology.
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