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Contrast‐induced encephalopathy following cardiac catheterization
Objectives To describe the epidemiology, pathophysiology, clinical presentation, and management of contrast‐induced encephalopathy (CIE) following cardiac catheterization. Background CIE is an acute, reversible neurological disturbance directly attributable to the intra‐arterial administration of io...
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Published in: | Catheterization and cardiovascular interventions 2017-08, Vol.90 (2), p.257-268 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Objectives
To describe the epidemiology, pathophysiology, clinical presentation, and management of contrast‐induced encephalopathy (CIE) following cardiac catheterization.
Background
CIE is an acute, reversible neurological disturbance directly attributable to the intra‐arterial administration of iodinated contrast medium.
Methods
The PubMed database was searched and all cases in the literature were retrieved and reviewed.
Results
52 reports of CIE following cardiac catheterization were found. Encephalopathy, motor and sensory disturbances, vision disturbance, opthalmoplegia, aphasia, and seizures have been reported. Transient cortical blindness is the most commonly reported neurological syndrome, occurring in approximately 50% of cases. The putative mechanism involves disruption of the blood brain barrier and direct neuronal injury. Contrast‐induced transient vasoconstriction has also been implicated. Symptoms typically appear within minutes to hours of contrast administration and resolve entirely within 24–48 hr. Risk factors may include hypertension, diabetes mellitus, renal impairment, the administration of large volumes of iodinated contrast, percutaneous coronary intervention or selective angiography of internal mammary grafts, and previous adverse reaction to iodinated contrast. Characteristic findings on cerebral imaging include cortical and sub‐cortical contrast enhancement on computed tomography (CT). Imaging findings in CIE may mimic subarachnoid hemorrhage or cerebral ischemia; the Hounsfield scale on CT and the apparent diffusion coefficient on magnetic resonance imaging (MRI) are useful imaging tools in distinguishing these entities. In some cases, brain imaging is normal. Prognosis is excellent with supportive management alone. CIE tends to recur, although re‐challenge with iodinated contrast without adverse effects has been documented.
Conclusions
CIE is an important clinical entity to consider in the differential diagnosis of stroke following cardiac catheterization. Given that prognosis is excellent with supportive management only, physicians should be aware of it, and consider it prior to initiating thrombolysis. © 2016 Wiley Periodicals, Inc. |
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ISSN: | 1522-1946 1522-726X |
DOI: | 10.1002/ccd.26871 |