Abstract 276: Contrast‐Induced Neurotoxicity Manifesting as Hemorrhagic Complications following Diagnostic Cerebral Angiography: A Common Proposed Pathophysiologic Mechanism

Introduction Digital Subtraction Angiography (DSA) is the gold standard for intracranial cerebral vasculature imaging. Complications are unusual, but when they do occur, they can result in substantial morbidity. Contrast‐induced neurotoxicity (CIN) has been a rare, incompletely described phenomenon presumed to be caused by disruption of the blood‐brain barrier (BBB) or endothelial injury with ensuing seizures, cerebral edema, or pseudo‐subarachnoid hemorrhage. We report two patients with acute neurological deterioration following DSA complicated by hemorrhage, suggesting a common pathologic process of BBB injury and vascular instability. Materials and Methods Case 1: A 54‐year‐old woman with coronary artery disease on aspirin presented with non‐traumatic multicompartmental hemorrhage of the right frontoparietal lobes and basal ganglia bilaterally with cortical, subarachnoid, and parafalcine subdural hemorrhages. Non‐invasive imaging with CT arteriogram, CT venogram, and magnetic resonance imaging (MRI) did not reveal any underlying etiology. DSA was performed with no aneurysm, arteriovenous malformation, dissection, or venous thrombosis to explain the patient's clinical presentation. Post‐procedure, the patient promptly worsened with growing subarachnoid hemorrhage, ventricular dilation, and new neurologic deficits. Retrospective angiographic assessment revealed subtle multifocal arterial narrowing and vessel beading, predominantly within the distal anterior cerebral artery branches, supportive of underlying RCVS with further endothelial disruption possibly caused by intra‐arterial contrast administration. Case 2: A 65‐year‐old woman with incidentally found asymptomatic high‐grade right internal carotid stenosis on clopidogrel underwent elective DSA. Immediately post‐procedure, the patient experienced right shoulder twitching, headache, followed by generalized seizure and unresponsiveness. She was stabilized in the intensive care unit. Interval CT showed diffuse hyperdensities raising suspicion of contrast extravasation or hemorrhage. MRI confirmed multicompartmental hemorrhage. Repeated non‐invasive imaging did not show an aneurysm or any other explanation for the bleeding. She ultimately required external ventricular drain placement for cerebrospinal fluid diversion and intracranial hypertension management with high‐dose steroids and hypertonic saline. Neurologic function was progressively restored, and she was ambulatory on day seven. The patient had completely recovered at the 6‐month follow‐up. Results In each of the two patients, DSA was technically successful with no vascular injury, but both had immediate post‐procedure worsening in the form of hemorrhage, edema, and/or seizure. Imaging revealed true subarachnoid blood in each of the two cases without iatrogenic injury, aneurysm, arteriovenous malformation, or coagulopathy to account for the bleeding. Each case contained characteristics of acute BBB failure and endothelial damage due to intra‐arterial exposure of elevated osmolar contrast in the form of hemorrhagic neurotoxicity. Conclusion These cases detail a rare but serious complication of DSA in which contrast‐induced neurotoxicity appears to extend beyond pseudo‐subarachnoid hemorrhage to true hemorrhagic events. The shared pathway may involve acute disruption of the BBB and damage to the endothelium, furthered by procedure‐related hemodynamic stress or vasoconstrictive stimuli. Early warning signs, such as focal twitching, headache, or depressed level of consciousness should be recognized and alert proceduralists towards CIN as a potential differential. Prompt imaging, intensive management of intracranial hypertension, and supportive therapy are the foundations of recovery. Further studies should elucidate the pathophysiology of BBB disruption in the context of hyperosmolar contrast‐induced neurotoxicity.