Contrast-Induced Encephalopathy

An 86-year-old female patient was admitted with acute posterolateral ST elevation myocardial infarction in the setting of triple-vessel coronary artery disease. Coronary angiography was performed with 190 mL Ultravist 370. In the peri-interventional period, reduced alertness (somnolence, GCS 12), left-sided hemiparesis, and bilateral signs of pyramidal tract dysfunction (Babinski reflex) were noted. Imaging with native computed tomography on the same day enabled visualization of cortical hyperdensity and cortical edema (Figures a and b). Neither could be visualized on the following day. Electroencephalography revealed severe diffuse slowing without epilepsy-typical potentials. A trial attempt at treatment with levetiracetam, an antiepileptic drug (500 mg 1–0–1), was undertaken. After 72 h, neurological symptoms were improving. We assumed the case to be one of contrast-induced encephalopathy. With an incidence of 0.3–2%, this condition is very rare. From a pathophysiological perspective, it involves direct neurotoxicity with damage to the blood–brain barrier and endothelial dysfunction. Hypertension, diabetes, kidney failure, large volumes of contrast, and male sex are considered to be risk factors. Symptoms usually resolve spontaneously and completely (after 24–72 h). Where possible, the re-use of contrast should be avoided.

Figure.

a) Prominent bilateral hyperdensity in the frontoparietal networks left > right (arrows), DDx: subarachnoid hemorrhage, DDx: contrast residue; b) signs of cortical edema, corticomedullary boundary obliteration (asterisks)

Institut für Radiologie, Neuroradiologie und Nuklearmedizin, Klinikum Darmstadt.