Abstract TP381: De novo cerebral vascular malformations in hepatic cirrhosis: a case series and single center experience.

Introduction: Cerebral AVMs are usually considered congenital, but this has been challenged by reports of de novo AVM. Chronic liver disease is associated with vascular remodeling in the liver and systemically, including pathological neovascularization which may drive aberrant angiogenesis in distant organs such as the brain. We describe 3 patients at our center with alcoholic cirrhosis who presented with intracranial hemorrhage from AVM or cerebral proliferative angiopathy. Methods: PubMed search of case reports and series. Results: Patient 1 43-year-old male with decompensated cirrhosis and epilepsy presented with breakthrough seizure, found to have left parietal ICH. Admission coagulopathy was corrected. Had craniotomy due to hematoma expansion. Exam declined in a week; imaging showed bilateral convexity SAH. Transferred to our center, DSA showed ruptured SM grade 2 AVM of left parietooccipital region (MCA/PCA feeders, superficial drainage). Also unruptured SM grade 3 AVM of left frontotemporal region. Discharged with plan for SRS. Two years earlier he presented with right hemiparesis thought to be Todd’s paresis; MRI then showed no vascular lesions. Patient 2 43-year-old female with cirrhosis, amphetamine use, prior right frontal ICH, and epilepsy presented with breakthrough seizures due to acute left frontal IPH. MRI showed hemorrhages and no significant lesions. INR 1.5, platelets 84K. DSA showed lenticulostriate arterial shunting into the galenic vein, supporting proliferative angiopathy. Also 2.5 mm aneurysm from distal left callosomarginal artery, likely source of hemorrhage. Underwent craniotomy for hematoma evacuation and aneurysm occlusion. Patient 3 39-year-old male with cirrhosis and systemic complications admitted for L5-S1 discitis due to MSSA bacteremia, later developed acute left hemiparesis. Initial CT showed right frontal IPH. MRI showed enhancing lesion in right sylvian fissure near the hematoma. DSA showed arteriovenous shunting lesion in the right sylvian fissure, suggestive of proliferative angiopathy. Additional lesions in left scalp supplied by STA. Days later, patient had new left occipital ICH with IVH and passed. Conclusions: Chronic liver disease, fibrosis, and compensatory angiogenesis generate a systemic proangiogenic environment facilitating vascular remodeling, including formation of de novo cerebral vascular malformations. This rare association is supported by clinical reports and mechanistic parallels in angiogenesis pathways.