Lauren Peruski, DO
You’re called to the bedside of a patient who, just hours prior, was recanalized through a successful endovascular thrombectomy. The patient has worsened by more than four points on the NIH Stroke Scale, in addition to worsening by more than two points on the Glasgow Coma Scale, since their last neurologic assessment. You consider the numerous, known complications of post-endovascular thrombectomy care, including reperfusion injury, hemorrhagic transformation of infarcted tissue, artery perforation/dissection, and recurrent ischemic stroke. Repeat vessel imaging confirms vessel integrity. MRI of the brain shows edematous change extending beyond the infarct core, accompanied by contrast staining. Over the next two weeks, the patient recovers from these deficits, and continues to improve from a stroke standpoint as well.
This case provides an example of contrast-induced encephalopathy (CIE), which is a rare neurologic complication that occurs during or after the use of contrast medium in various angiographic procedures. It is suspected that CIE occurs secondary to a number of mechanisms including underlying blood-brain barrier disruption, hyperosmolarity, and direct neurotoxicity from contrast medium. Clinically, patients with CIE may experience encephalopathy, motor or sensory deficits, visual disturbance, aphasia, or seizures within hours of EVT. In this brief report, the incidence and risk factors of CIE were examined in patients who underwent endovascular thrombectomy (EVT).
CIE was defined using specified clinical and radiologic criteria within 24 hours of EVT. Clinical criteria included an increase of ³4 on the NIH Stroke Scale or a decrease of ³2 on the Glasgow Coma Scale. As an alternative, patients were allowed to be examined in this study if they displayed delayed improvement after EVT that was unexplainable by an alternate etiology. Radiologic criteria were defined as edematous change extending beyond the infarct core accompanied by contrast staining.
Between September 2014 and December 2019 at two tertiary hospitals, 421 patients received EVT, and seven patients were diagnosed with CIE (incidence of 1.7%). The main risk factors identified were renal dysfunction and history of previous stroke. Follow up imaging revealed resolution of cerebral edema, with a time to recovery ranging between two days to several weeks. These patients were managed with “supportive” care; however, the treatment of CIE was beyond the scope of this publication.
To summarize, CIE should be on the differential diagnosis for any patient who worsens clinically following EVT, and who has imaging consistent with contrast staining and edematous changes. Suspicion should be especially high in those patients with a history of previous stroke or renal disease, as these are risk factors for the development of CIE.