Contrast-induced encephalopathy (CIE) is a rare but well-known complication of mostly intra-arterial contrast administration and presents with a variety of neurological deficits due to disruption of the blood-brain barrier. We present a case of CIE after administration of intravenous contrast for computed tomography pulmonary angiogram (CTPE). A woman in her mid-70s with history of chronic obstructive pulmonary disease (COPD) presented with progressively worsening shortness of breath. She was diagnosed with multifocal pneumonia and started on IV antibiotics, IV steroids, and bilevel positive airway pressure (BiPAP) ventilation. A CTPE was done to rule out a pulmonary embolism during which she received 100 cc of Isovue 370 (iopamidol 76%), a low-osmolar, non-ionic, monomeric, iodine-based contrast agent. Within minutes of the contrast administration, the patient developed confusion and agitation with elevated blood pressure. Neurological evaluation revealed no gross focal motor or cranial nerve deficits and bilateral 2+ reflexes with mute plantar reflexes. Laboratory investigations were unchanged. She was shifted to the ICU but continued to remain drowsy and disoriented. CT brain done within two hours of onset revealed no intracranial abnormality. She was managed conservatively with IV fluids, neuro-checks, and blood pressure control. Her sensorium improved within 48 hours with supportive treatment. Repeat neuroimaging was not performed. She was discharged after four days with the resolution of her respiratory symptoms. CIE is a known but uncommon complication associated with the use of intraarterial contrast media but has been found to occur even after intravenous administration, which has been reported only once in literature. The presentation is highly variable, ranging from headache to coma, with transient cortical blindness being the most commonly identified. The diagnosis requires a high index of suspicion, and brain imaging is usually pathognomonic; however, cases in the absence of radiological signs have also been diagnosed. Typically, symptoms resolve within 48-72 hours and the disease runs a benign course, but cases of persistent neurological deficit and even cases of fatal cerebral edema have been reported.Treatment is usually supportive with intravenous hydra-tion and anticonvulsants and the occasional use of IV steroids and mannitol with favorable outcomes.
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