Abstract 49: Diagnostic Yield of Catheter Angiography in Patients with Subarachnoid Hemorrhage and Negative Initial Non-Invasive Neurovascular Examinations

Abstract

Purpose: To determine the yield of catheter angiography for the detection of causative vascular lesions in patients with subarachnoid hemorrhage (SAH) who have a negative initial non-invasive neurovascular examination. Methods: Between January 1st, 2006 and August 1st, 2011, we instituted a prospective protocol by which patients who presented to our institution with SAH and had a negative initial non-invasive neurovascular examination (CT or MR angiogram [CTA, MRA]) were examined with catheter angiography to detect causative vascular lesions. Two experienced neuroradiologists evaluated the NCCTs to determine the pattern of SAH (diffuse, perimesencephalic or peripheral) and the catheter angiograms to assess for the presence of a causative vascular lesion. All differences in reader interpretation were resolved by consensus. Results: Forty-eight patients were included in our study, with a mean age of 58 years (median 59 years, range 25-84 years). Twenty-six patients were male (54.2%) and 22 female (45.8%). Twenty-eight patients had diffuse SAH (58.3%), 11 peripheral SAH (22.9%) and 9 perimesencephalic SAH (18.8%). The initial non-invasive neurovascular examination was a CTA in 41 patients (85.4%) and an MRA in 7 patients (14.6%). A second catheter angiogram was performed in 30 patients (62.5%). Mean time interval between the initial non-invasive neurovascular examination and the first catheter angiogram was 0.9 days (median 1 day, range 0-7 days) and the second catheter angiogram was 12.2 days (median 8.5 days, range 4-69 days). Catheter angiography demonstrated a causative vascular lesion in 4 patients (8.3%), 3 of which had diffuse SAH (yield of 10.7%) and 1 had peripheral SAH (yield of 9.1%). Of note, 1 of the causative vascular lesions was identified in a second catheter angiogram performed 8 days after the CTA in a patient with diffuse SAH. The vascular lesions identified were 2 dural arteriovenous fistulas, 1 pial cerebellopontine angle arteriovenous malformation with a 2-mm feeding artery aneurysm located in the internal auditory canal ( Figure ), and a 3-mm anterior communicating artery aneurysm. Two of the vascular lesions underwent endovascular embolization, 1 radiosurgery and 1 endovascular embolization followed by radiosurgery. In retrospect, the vascular lesion could be seen in the initial examination in 2 patients. Conclusion: Catheter angiography is a valuable tool in the evaluation of patients with diffuse and peripheral SAH who have a negative initial non-invasive neurovascular examination, demonstrating a causative vascular lesion in 10.7% and 9.1% of patients, respectively.