J J Heit1, G T Pastena2, R G Nogueira3, A J Yoo4, T M Leslie-Mazwi5, J A Hirsch1, J D Rabinov6. 1. From the Department of Radiology (J.J.H.), Interventional Neuroradiology Division, Stanford University Hospital, Stanford, California. 2. Department of Radiology (G.T.P.), Albany Medical Center, Albany, New York. 3. Departments of Neurology, Neurosurgery, and Radiology (R.G.N.), Emory University School of Medicine, Marcus Stroke and Neuroscience Center, Atlanta, Georgia. 4. Texas Stroke Institute (A.J.Y.), Plano, Texas. 5. Department of Neuroradiology and Interventional Neuroradiology (T.M.L.-M., J.A.H., J.D.R.), Massachusetts General Hospital, Boston, Massachusetts. 6. From the Department of Radiology (J.J.H.), Interventional Neuroradiology Division, Stanford University Hospital, Stanford, California jrabinov@partners.org.
Abstract
BACKGROUND AND PURPOSE: CT angiography is increasingly used to evaluate patients with nontraumatic subarachnoid hemorrhage given its high sensitivity for aneurysms. We investigated the yield of digital subtraction angiography among patients with SAH or intraventricular hemorrhage and a negative CTA. MATERIALS AND METHODS: An 11-year, single-center retrospective review of all consecutive patients with CTA-negative SAH was performed. Noncontrast head CT, CTA, DSA, and MR imaging studies were reviewed by 2 experienced interventional neuroradiologists and 1 neuroradiologist. RESULTS: Two hundred thirty patients (mean age, 54 years; 51% male) with CTA-negative SAH were identified. The pattern of SAH was diffuse (40%), perimesencephalic (31%), sulcal (31%), isolated IVH (6%), or identified by xanthochromia (7%). Initial DSA yield was 13%, including vasculitis/vasculopathy (7%), aneurysm (5%), arteriovenous malformation (0.5%), and dural arteriovenous fistula (0.5%). An additional 6 aneurysms/pseudoaneurysms (4%) were identified by follow-up DSA, and a single cavernous malformation (0.4%) was identified by MRI. No cause of hemorrhage was identified in any patient presenting with isolated intraventricular hemorrhage or xanthochromia. Diffuse SAH was due to aneurysm rupture (17%); perimesencephalic SAH was due to aneurysm rupture (3%) or vasculitis/vasculopathy (1.5%); and sulcal SAH was due to vasculitis/vasculopathy (32%), arteriovenous malformation (3%), or dural arteriovenous fistula (3%). CONCLUSIONS: DSA identifies vascular pathology in 13% of patients with CTA-negative SAH. Aneurysms or pseudoaneurysms are identified in an additional 4% of patients by repeat DSA following an initially negative DSA. All patients with CT-negative SAH should be considered for DSA. The pattern of SAH may suggest the cause of hemorrhage, and aneurysms should specifically be sought with diffuse or perimesencephalic SAH.
BACKGROUND AND PURPOSE: CT angiography is increasingly used to evaluate patients with nontraumatic subarachnoid hemorrhage given its high sensitivity for aneurysms. We investigated the yield of digital subtraction angiography among patients with SAH or intraventricular hemorrhage and a negative CTA. MATERIALS AND METHODS:An 11-year, single-center retrospective review of all consecutive patients with CTA-negative SAH was performed. Noncontrast head CT, CTA, DSA, and MR imaging studies were reviewed by 2 experienced interventional neuroradiologists and 1 neuroradiologist. RESULTS: Two hundred thirty patients (mean age, 54 years; 51% male) with CTA-negative SAH were identified. The pattern of SAH was diffuse (40%), perimesencephalic (31%), sulcal (31%), isolated IVH (6%), or identified by xanthochromia (7%). Initial DSA yield was 13%, including vasculitis/vasculopathy (7%), aneurysm (5%), arteriovenous malformation (0.5%), and dural arteriovenous fistula (0.5%). An additional 6 aneurysms/pseudoaneurysms (4%) were identified by follow-up DSA, and a single cavernous malformation (0.4%) was identified by MRI. No cause of hemorrhage was identified in any patient presenting with isolated intraventricular hemorrhage or xanthochromia. Diffuse SAH was due to aneurysm rupture (17%); perimesencephalic SAH was due to aneurysm rupture (3%) or vasculitis/vasculopathy (1.5%); and sulcal SAH was due to vasculitis/vasculopathy (32%), arteriovenous malformation (3%), or dural arteriovenous fistula (3%). CONCLUSIONS: DSA identifies vascular pathology in 13% of patients with CTA-negative SAH. Aneurysms or pseudoaneurysms are identified in an additional 4% of patients by repeat DSA following an initially negative DSA. All patients with CT-negative SAH should be considered for DSA. The pattern of SAH may suggest the cause of hemorrhage, and aneurysms should specifically be sought with diffuse or perimesencephalic SAH.
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