Clinical and imaging features of contrast induced neurotoxicity after cerebral angiography – Case series (P5.3-053)

Objective: To describe the clinical and imaging characteristics of nine consecutive patients who developed Contrast Induced Neurotoxicity. Background: Contrast Induced Neurotoxicity (CIN) is an uncommon complication that occurs from iodinated contrast penetration through the blood-brain barrier. Predisposing factors remain unknown. Design/Methods: Retrospective review of a prospectively collected neurointerventional data base was performed from January 2015 to July 2018. Demographics, past medical history, clinical presentation and radiological signs of patients who developed presumed CIN were collected. Results: Nine of 1468 patients from 2027 procedures were identified. Median age was 75 years (IQR 63–78). 7/9 had hypertension and hyperlipidemia. Six patients underwent aneurysm embolization, one for carotid artery stenting and two diagnostic DSA. Median procedure time was 100 minutes (IQR 91–123). Isovue-300 was used in all except two cases (elevated creatinine) where Visipaque-320 was used (contrast median of 109cc (IQR 100–125cc)). All patients presented elevated intervals of SBP ranging between 150–200 mmHg during the procedure. Mean symptom onset was six hours post-procedure with aphasia (six patients), encephalopathy (five), motor weakness (four), neglect (two) and cortical blindness (two). All the patients had head CT performed shortly after the symptoms onset. It demonstrated loss of gray-white matter differentiation (six), sulcal effacement (five) and contrast extravasation (two). CTP demonstrated prolonged MTT with mildly decreased CBF in three patients with patent intracranial vasculature. No laboratory abnormality was found in any of the patients. EEG performed in 4 patients demonstrated diffuse ipsilateral dysfunction without epileptiform activity. All patients received intravenous fluids and steroids with symptom resolution within 72 hours in 8/9 (88%). Conclusions: CIN should be considered in the context of progressive onset of neurological deficits after endovascular procedures. A distinct imaging pattern of ipsilateral hemisphere edema in the absent of acute ischemia is usually identified. Uncontrolled procedural hypertension seems to be a predisposing factor for all these patients. Disclosure: Dr. Zevallos has nothing to disclose. Dr. Dandapat has nothing to disclose. Dr. Lopez Cardenas has nothing to disclose. Dr. Holcombe has nothing to disclose. Dr. Asi has nothing to disclose. Dr. Samaniego has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Microvention/Medtronic. Dr. Ansari has nothing to disclose. Dr. Mendez Ruiz has nothing to disclose. Dr. Dai has nothing to disclose. Dr. Ortega-Gutierrez has nothing to disclose.