Iodinated contrast-induced encephalopathy: imaging findings, clinical correlation and differential diagnosis the radiologist needs to know.

Congress:

ECR 2020

Poster Number:

C-07985

Type:

Educational Exhibit

Keywords:

Neuro, Contrast agents, Interventional vascular, Neuroradiology brain, Catheter arteriography, CT, MR, Diagnostic procedure, Embolisation, Acute, Toxicity, Not applicable, Performed at one institution

Authors:

A. Bartolo¹, A. PEDICELLI², A. Alexandre¹, F. Giubbolini³, I. Valente¹, E. Lozupone⁴, F. D'Argento⁵, C. Colosimo⁴; ¹Roma/IT, ²ROMA (RM)/IT, ³Siena /IT, ⁴ROME/IT, ⁵Taviano (LE)/IT

DOI:

10.26044/ecr2020/C-07985

DOI-Link:

https://dx.doi.org/10.26044/ecr2020/C-07985

Fig. 2: 71-years old male presented to emergency department with a subarachnoid...

Fig. 3: 72-years old female with a fusiform dissecting aneurysm of the right posterior...

Fig. 4: 61-years old female with a saccular aneurysm of the left anterior cerebral...

Fig. 5: 70-years old male with a stenosis of the left carotid artery, treated with...

Findings and procedure details

Imaging findings may be subtle.

A non-contrast brain CT is usually performed at the time of symptoms onset, in order to rule out other main causes of an acute neurologic deficit (especially more urgent and frequent events, such as embolism). The typical pattern consist of variable cortical and subarachnoid hyperdensity, associated with mass effect due to oedema. This pattern of “gyriform” hyperdensity is thought to be caused by contrast leakage, related to focal blood–brain barrier disruption.

After CIE diagnosis, the patient is generally transferred to the intensive care unit, and treated with anti-oedemic drugs such as mannitol and corticosteroids.

A new brain CT is usually performed about 24-48 hours later, to confirm a total/subtotal decrease of previous alterations. In most cases this is associated with a dramatic improvement of the neurological deficit (Fig. 2, Fig. 3, Fig. 4).

MR imaging shows T2-w/FLAIR cortical/subcortical hyperintensity in the affected region, a corresponding slight DWI hyperintensity without any change on the apparent diffusion coefficient (ADC) maps (Fig. 5). These findings usually completely disappear after 48-72 hours.

In the correct clinical context, differential diagnosis should include subarachnoid hemorrhage and evolving cerebral infarction. Clinical examination and correct imaging interpretation are crucial to identify the CIE.

Clinical conditions may vary from affected territory and eloquent brain areas involved. Symptoms may include: transient cortical blindness, seizure, focal neurological deficits (hemiparesis, aphasia, loss of coordination), confusion, psychomotor agitation, dysmetria, seizure and coma.

Neurological symptoms usually resolve completely within 24-48 hours.

Predisposing factors leading to CIE are chronic hypertension, transient ischemia attack (TIA), impaired cerebral autoregulation, impaired renal function and large contrast volumes.

An history of hypertension, particularly, seems to be associated to cerebral autoregulatory dysfunction, leading to blood–brain barrier injury.